Step 2 4 Px

Front 1

What is the typical complaint of a pt with retinal detachment?

Back 1

Sudden painless onset of flashing lights
Floaters
“shade comes down” over the vision of one eye

Front 2

What is the treatment for benign paroxysmal positional vertigo (BPPV)?

Back 2

Epley maneuver (reposition otolith)

Front 3

What is Todd’s paralysis?

Back 3

Post-ictal hemiparesis lasting 15-24hrs

Front 4

List examples of SSRIs

Back 4

Fluoxetine (Prozac)
Sertraline (Zoloft)
Paroxetine (Paxil)
Fluvoxamine (Luvox, Lescol)
Citalopram (Celexa)
Escitalopram (Lexapro)

Front 5

List examples of Tricyclic Antidepressants (TCAs)

Back 5

Imipramine (Tofranil)
Amitriptyline (Elavil)
Desipramine (Norpramin)
Nortriptyline (Aventyl)
Clomipramine (Anafranil)
Doxepin (Silenor, Sinequan)

Front 6

List examples of MAOIs

Back 6

Phenelzine (Nardil)
Tranylcypromine (Parnate)
Selegiline (Eldepryl, Emsam, Zelapar)

Front 7

List example of NDRI

Back 7

Buproprion (wellbutrin)

Front 8

List examples of SNRI

Back 8

Venlafaxine (Effexor, Pristiq)
Duloxetine (Cymbalta)
Milnacipran (Savella)
Nefazodone (Serzone)

Front 9

list examples of tetracyclic antidepressants

Back 9

Mirtazapine (Remeron)
Trazodone (Desyrel, Oleptro

Front 10

What drugs, when combined with SSRIs are known for causing Serotonin syndrome?

Back 10

SSRIs, SNRIs, MAOIs
LSD, St. John’s wort, Levodopa, Meperidine, Lithium
Amphetamines, cocaine, ectasy

Front 11

What is the most common cause of sensorineural hearing loss? What is the most common cause of conductive hearing loss?

Back 11

Sensorineural → presbycusis
Conductive → otosclerosis

Front 12

What is the most common complication of recurrent otitis media?

Back 12

hearing loss

Front 13

An elderly pt presents to the ED with a HA & dilated right pupil. During the history, she reports that she fell at home 5 days ago. What is the most likely diagnosis?

Back 13

R-sided subdural hematoma

Front 14

What medications other than stimulants are used in the treatment of ADHD?

Back 14

TCAs, Bupropion, α-2 agonists (clonidine)

Front 15

What medications are used in the treatment of Tourette’s syndrome?

Back 15

Fluphenazine (Permitil, Prolixin)
Pimozide (Orap)
Tetrabenazine (Xenazine)

Front 16

What are the most worrisome side effects of the ADHD drug atomoxetine?

Back 16

↑ suicidal ideation
liver injury

Front 17

What is the definitive tx for an epidural or subdural hematoma?

Back 17

Evacuation of the hematoma with a burr hole

Front 18

What serum lab abnormalities might you see in a pt with bacterial meningitis? (SU pg 169)

Back 18

↑ WBC ct, left shift or bandemia, leucopenia, hypOnatremia

Front 19

A pt comes to the clinic with the c/o hearing loss and vertigo. On exam of the tympanic membrane you note a grayish-white “pearly” lesion involving the TM. What is the dx?

Back 19

cholesteatoma

Front 20

What anti-islet antibodies can be seen in pts with Type 1 DM?

Back 20

Anti-insulin (IAA)
Anti-islet cell cytoplasm (ICA)
Anti-glutamic acid decarboxylase (GAD)
Anti-tyrosine phosphatase (IA-2)

Front 21

How do you distinguish the somogyi effect from the Dawn phenomenon?

Back 21

Somogyi: at 2-3 am, will have low blood glucose
Tx: ↓ evening insulin
Dawn: at 2-3 am will have high blood glucose
Tx: ↑ evening insulin

Front 22

A concerned mother brings her 6yo son to see you. He c/o nausea and has been vomiting. The mother says that she thinks he caught a stomach bug. What might the child have instead?

Back 22

Diabetic ketoacidosis (DKA)

Front 23

What must be kept in mind for a type I diabetic pt that plans to begin a strenuous exercise program?

Back 23

↑ exercise causes muscle to uptake more glucose
pt is at risk of hypoglycemia

Front 24

Whch type of insulin is used in continuous infusion insulin pumps & in treatment of DKA?

Back 24

Regular or fast acting insulin

Front 25

Describe the basic mechanism behind the Somogyi effect

Back 25

Evening insulin dose is too high, blood sugar bottoms out an hour or two past midnight
Stress hormones are released in response to the very low blood sugar → morning glucose is elevated

Somogyi: at 2-3 am, will have low blood glucose
Tx: ↓ evening insulin
Dawn: at 2-3 am will have high blood glucose
Tx: ↑ evening insulin

Front 26

Describe the mechanism behind the Dawn phenomenon

Back 26

Very elevated morning blood sugar, evening insulin dose is too low
Blood sugar is inadequately treated so it continues to ↑ throughout the night

Somogyi: at 2-3 am, will have low blood glucose
Tx: ↓ evening insulin
Dawn: at 2-3 am will have high blood glucose
Tx: ↑ evening insulin

Front 27

How can you differentiate between the Somogyi effect & Dawn phenomenon?

Back 27

Check blood sugar in middle of night (2-4am)

Front 28

What Diabetic drug:
Lactic acidosis is a rare but worrisome side effect

Back 28

Metformin

Front 29

What Diabetic drug:
Most common side effect is hypoglycemia

Back 29

Sulfonylureas (Glipizide, Gliburide, tolbutamide)

Front 30

What Diabetic drug:
Oldest & cheapest of the oral agents

Back 30

Sulfonylureas (Glipizide, Gliburide, tolbutamide)

Front 31

What Diabetic drug:
Often used in combination with any of the other oral agents

Back 31

Metformin

Front 32

What Diabetic drug:
Also help lower TGs and LDL cholesterol levels

Back 32

Metformin

Front 33

What Diabetic drug:
Not safe in settings of CHF

Back 33

Thiazolidinediones (TZDs, “glitazones”)

Front 34

What Diabetic drug:
Should not be used in pts with ↑ serum Cr

Back 34

Metformin & Sulfonylureas (Glipizide, Gliburide, tolbutamide)

Front 35

What Diabetic drug:
Should not be used in pts with inflammatory bowel disease

Back 35

α-glucosidase inhibitors (acarbose)

Front 36

What Diabetic drug:
Hepatic serum transaminase (LFTs) levels should be carefully monitored

Back 36

Thiazolidinediones (TZDs, “glitazones”) and Sulfonylureas (Glipizide, Gliburide, tolbutamide)

Front 37

What Diabetic drug:
Not associated with weight gain, often used in overweight diabetics

Back 37

Metformin

Front 38

What diabetic drug:
Metabolized by liver, excellent choice in pts with renal dz

Back 38

Thiazolidinediones (TZDs, “glitazones” – rosi & pio)

Front 39

What diabetic drug:
Primarily effects postprandial hyperglycemia, taken with meals

Back 39

α-glucosidase inhibitors (acarbose)

Front 40

What are the differences between the newer diabetic agents?

Back 40

Sitagliptin (Januvia), Saxagliptin (Onglyza)
Inhibitors of dipeptyl peptidase IV (DPP-4) which affects glucagon-like peptide (GLP-1) aka incretins
Prolongs incretin actions, which ↓ glucagon secretion and ↑ insulin secretion, delays gastric emptying

Exenatide (byetta), liraglutide (victoza)
Exenatide is an analog of exendin, a hormone derived from Glia monster saliva, with actions similar to GLP-1
Lirglutide is a synthetic analog of human GLP-1
Mimic the actions of incretins, which ↓ glucagon secretion and ↑ insulin secretion, delay gastric emptying
Not approved for use while on insulin therapy
AE: possibly ↑ risk of acute pancreatitis

Pramlintide (Symlin)
Amylin analog, normally secreted with insulin, ↓ glucagon secretion and gastric emptying
Used only in pts taking insulin but in either Type I or II DM

Front 41

What are the criteria for the diagnosis of Metabolic Syndrome?

Back 41

Diagnosis based on any 3 of the following:
Abdominal/ truncal obesity: waist circumference >40in (102cm) in men or >35 (88cm) in women
TG > 150
HDL <40 in men, < 50 in women
BP > 130/ 85
Fasting serum glucose > 100 (or 2hr post oral glucose >140)

Front 42

What skin finding can be a sign of insulin resistance?

Back 42

Acanthosis nigricans

Front 43

Hyperosmolar Hyperglycemia Non-ketotic coma (HHNK) is similar in presentation to DKA but differs in what important ways?

Back 43

Occurs only in Type 2 DM
Blood sugar more likely > 800
Lacks ketoacidosis

Front 44

You have a well-controlled DM II pt who needs a CT scan with IV contrast. What medication is this pt likely on that must be temporarily held?

Back 44

Metformin

Front 45

Whats the MOA of
α-glucosidase inhibitors (acarbose)

Back 45

↓ GI absorption of starch & disaccharides

Front 46

Whats the MOA of Sulfonylureas (Glipizide, Gliburide, tolbutamide)
& Meglitinides

Back 46

Stimulates insulin release

Front 47

Whats the MOA of Metformin

Back 47

↓ hepatic gluconeogenesis

Front 48

Whats the MOA of Thiazolidinediones (TZDs, “glitazones” – rosi & pio)

Back 48

↑ tissue glucose uptake and improves insulin sensitivity

Front 49

Whats the MOA of Exenatide & Liraglutide

Back 49

↓ glucagon, ↑ insulin,

Front 50

Whats the MOA of Sitagliptin & Saxagliptin

Back 50

Inhibits DPP-V:
↓ glucagon, ↑ insulin,
delays gastric emptying

Front 51

Whats the MOA of Pramlintide?

Back 51

An amylin analog which
↓ glucagon & delays gastric empyting

Front 52

Which diabetic drugs may cause hypoglycemia?

Back 52

Sulfonylureas (Glipizide, Gliburide, tolbutamide)
Meglitinides

Front 53

Which diabetic medications should be avoided in pts with heart failure?

Back 53

Thiazolidinediones (TZDs, “glitazones”)

Front 54

what are the common causes of DKA?

Back 54

Common causes of DKA: usually excess of glucagon, catecholamines, or corticosteroids
Infection (pneumonia, gastroenteritis, UTI)
Medication reduction or omission
Severe medical illness (MI, CVA, trauma)
Undiagnosed DM
Dehydration
Alcohol or drug abuse
Corticosteroids

Front 55

What are the steps in the tx of Diabetic ketoacidosis (DKA)?

Back 55

Identify & tx underlying cause
Replace K+ , Ca2+ , Mg2+ & PO43-

Front 56

How do we diagnose diabetic gastroparesis?

Back 56

Gastric emptying study

Front 57

What are the treatment options for diabetic gastroparesis?

Back 57

Want to promote GI motility:
Erythromycin
Metoclopramide (Reglan)

Front 58

General Care of Diabetes Mellitus:

Back 58

Exercise: walking at least 2hr/wk ↓ mortality by 40%
Healthy diet
Daily FSBG documented & brought to clinic visit
Physical Exam q3-6mo with attention to BP (goal <130/80); weight loss, feet, waist circumference
HbA1c q 3mo if > 7.0, q6mo if < 7.0
Amer Diabetic Assoc goal <7.0
Amer Assoc of Clinical Endocrinologists goal <6.5
Urine mircoalbumin q3mo-1yr
24hr urine for protein, Cr, and CrCl is UA protein >100 or high serum Cr
Consider annual 24hr urine for protein, Cr, and CrCl
Lipid Panel q1 yr:
Goal total cholesterol < 150
Goal LDL < 100 (<70 if evidence of vessel disease): use statins or WelChol which has been shown to ↓ HgA1c by 0.47% in users of metformin monotherap
Goal HDL > 40 (men) >50 (women)
Niacin may worsen insulin resistance
Chem. 8 and UA q 1yr
Dilated eye exam (r/o retinopathy, glaucoma, cataracts) q1yr
Influenza vaccine q1yr
Pneumonia vaccine
Consider daily ASA 81 mg, ACE-I, statin (Atorvastatin(Lipitor) 10mg)

Front 59

In a pt being treated for DKA, what is used to determine when to shut off the insulin infusion?

Back 59

Anion gap – when it is back in the normal range, insulin drip can be stopped

Front 60

Which electrolyte should be given at the beginning of treatment for DKA b/c of its propensity to drop with insulin infusion in these pts?

Back 60

potassium

Front 61

What are Kussmaul respirations, and what is their physiologic purpose?

Back 61

Slow deep breathing (typically, but also can be rapid breathing)
Slower breathing w/ worsening acidosis
Purpose is to blow off CO2 & raise pH

Front 62

What is the best way to avoid diabetic retinopathy, nephropathy, and neuropathy?

Back 62

Control the diabetes – HbA1c < 7.0
ACE inhibitors or ARBs – to prevent nephropathy
Monitor for microalbuminuria
Control HTN
Annual dilated eye exam – to screen for retinopathy

Front 63

How can you track diabetic nephropathy in a diabetic pt?

Back 63

Check microalbumin at least annually

Front 64

What is the pattern & type of sensation lost in diabetic neuropathy?

Back 64

Stocking & glove distribution

Front 65

The surgical intern is called to the bedside of a post-surgical male diabetic pt b/c SOB. The pt denies CP, but cardiac enzymes and an EKG are ordered anyway which reveal an evolving MI. Why doesn’t the diabetic pt have more symptoms indicative of his MI?

Back 65

Sensory loss of diabetic neuropathy effects the nerves involved in angina of chest pain

Front 66

What is the treatment for thyroid storm?

Back 66

ICU admission due to high mortality
R/o infectious cause with blood & urine cx. Empiric antibiotics if infxn is suspected.
Hydrate fluid deficit aggressively (unless overt heart failure). Use glucose solutions and replace multivitamins
Digoxin if heart failure and/or atrial fibrillation (higher than normal doses may be required)
Tylenol for fever. Avoid aspirin which interferes with thyroid protein binding generating more free thyroid
β-blockers to control adrenergic stimulation
Propanolol IV until adequate tachycardia resolved (must be monitored with continuous EKG and BP monitor) then PO4- q4-6hrs
Esmolol IV infusion titrated to resolve tachycardia
Thionamide to block new hormone synthesis
Propylthiouracil (PTU) – blocks peripheral conversion of T4 to T3, usual DOC
Methimazole (Tapazole) – longer acting than PTU, does not block peripheral conversion of T4 to T3 ∴ ideally administered with iopanoic acid (not avail in US) which does this conversion
Iodine to block the release of T4 to T3 from the gland, dose at least 1 hour after thionamide to prevent the iodine from being used to create more thyroid hormone
Iodide (sodium iodide) IV q6hrs
Lugol’s solution PO4- (or to IVF) q 8hrs
SSKI (saturated solution of potassium iodide) 5 drops PO4- q6-8hrs
+/- Glucocorticoids to ↓ conversion of T4 to T3 and treat the autoimmune process in a hyperthyroid pt with Grave’s Disease

Front 67

Explain workup of a palpable thyroid nodule

Back 67

Check TSH, free T4, thyroid sono to measure size and assess for other nodules
If hyperthyroid → radionucleotide uptake scan
(no role for radionucleotide scan if euthyroid or hypothyroid)
hot nodule → treat as hyperthyroid
cold nodule → FNA
If hypOthyroid → replace thyroid hormone and monitor for ↓ in nodule size
If nodule persists after thyroid replacement → FNA
If euthyroid → FNA

Front 68

Why must β-blockers be used with caution in diabetic pts?

Back 68

β-blockers mask symptoms of hypoglycemia

Front 69

A pt came into the ER with AMS & you had to administer a glucose infusion empirically b/c there was not a way to determine the blood glucose in a timely fashion. Later it was discovered that the pt was in DKA and subsequently treated inappropriately. In this case was you action careless & harmful?

Back 69

no

Front 70

What is used to determine whether a pt’s hypoglycemia is due to too much insulin production by the body or from too much exogenous insulin administration?

Back 70

Measure C-peptide level

Front 71

What can cause total T4 levels to increase despite free T4 remaining normal?

Back 71

↑ TBG (as seen in pregnancy, OCP use)

Front 72

What is the pathophysiology of Grave’s disease?

Back 72

Autoimmune Abs stimulate TSH receptor of the thyroid, causing excess production & release of thyroid hormone

Front 73

A woman comes to your office c/o neck pain. On exam she is tender and mildly swollen in the thyroid region of the neck. She also reports having some mild anxiety, and at times her heart seems to race. How do you treat this pt’s disease?

Back 73

Dx: subacute thyroiditis
Tx: self-limiting, NSAIDs & β-blockers for symptom control

Front 74

How can Grave’s disease be cured?

Back 74

Tx: subtotal thyroidectomy or radioablation using radioactive iodine
PTU or methimazole are used until one of these is performed

Front 75

Toxic multinodular goiter & Plummer’s disease are similar in presentation and treatment for Grave’s disease. How are they different?

Back 75

Toxic multinodular goiter: thyroid scan will show the isolated sites (nodules) of excess TH production
Grave’s disease: entire thyroid will show ↑ uptake

Front 76

Hypothyroidism can present as what common symptom in a pt?

Back 76

Depression (check TSH)

Front 77

Which antibodies are used to help in the diagnosis of Hashimoto’s thyroiditis?

Back 77

Antimicrosomal & antithyroglobulin Abs

Front 78

A woman comes to your office c/o neck mass. On exam she is not tender but mildly swollen in the thyroid region of the neck. She also reports having some mild anxiety and at times her heart seems to race. How do you treat this pt’s disease?

Back 78

Dx: Hashimoto’s thyroiditis
Tx: Levothyroxine treatment (Synthroid)

Front 79

What is the most common form of thyroid carcinoma?

Back 79

Papillary thyroid carcinoma

Front 80

What are the 2 most common complications of a thyroidectomy?

Back 80

Damage to the recurrent laryngeal nerve
Accidental removal of the parathyroid glands which can cause hypocalcemia

Front 81

What is the workup for a thyroid nodule?

Back 81

see above

Front 82

Explain next steps following a FNA of a thyroid nodule

Back 82

- FNA follow-up:
- Malignant → needs surgery
- Benign → repeat thyroid sono q6mos- 1 yr to make sure no increase in size
- If ↑ size → repeat FNA
- Nondiagnostic → repeat FNA
- Intermediate → repeat thyroid sono in 6 mos
- Even if FNA if negative you cannot 100% r/o thyroid cancer. Explain to pt that there is still ~1% chance that this could be cancer and offer to let them choose btw q6mo US surveillance or removal of the nodule (partial vs total thyroidectomy)

Front 83

HYQ: Pt has exophthalmos → what is the most likely cause?

Back 83

Dx: Grave’s Disese – antibodies build up & cause inflammation

Front 84

HYQ: How is diabetic gastroparesis diagnosed & treated?

Back 84

Diagnosis made by gastric emptying study
Tx: Metoclopramide (Reglan)

Front 85

HYQ: In which of the following hyperthyroid diseases is radioactive iodine most likely to result in hypothyroidism: Graves Disease, toxic multinodular goiter, toxic adenoma?

Back 85

Treatment for Grave’s disease is almost always going to result in hypOthyroidism

Front 86

HYQ: What is the treatment of the most common cause of hyperthyroidism?

Back 86

Mcc of hyperthyroidism = Grave’s Disease
Tx: radionucleotide iodine (preferred), or surgery

Front 87

HYQ: What can cause hypoglycemia in a non-diabetic pt?

Back 87

** Diabetes does NOT cause hypoglycemia
Insulinoma
Insulin or sulfonylurea use (Factitious disorder, Munchausen’s disorder, Malingering)
Check C-peptide levels
Alcohol use (fasting)
Adrenal insufficiency

Front 88

HYQ: What are the S/S of diabetic ketoacidosis (DKA)?

Back 88

Kussmaul respirations
Weight loss
Polyuria
Polydipsia
Nausea & vomiting

Front 89

HYQ: What lab abnormalities necessitate obtaining thyroid function testing to r/o thyroid disease?

Back 89

Hyperlipidemia
Unexplained hyponatremia
↑ CPK

Front 90

HYQ: A pt with hypothyroidism and ↑ anti-TPO antibodies is at ↑ risk of which type of cancer?

Back 90

Thyroid lymphoma

Front 91

What's the likely cause of hyperthyroidism?
Extremely tender thyroid gland

Back 91

Subacute thyroiditis

Front 92

What's the likely cause of hyperthyroidism?
Pretibial myxedema

Back 92

Graves Disease

Front 93

What's the likely cause of hyperthyroidism?
Pride in recent weight loss, medical professional

Back 93

Abusing levothyroxine

Front 94

What's the likely cause of hyperthyroidism?
Palpation of single thyroid nodule

Back 94

Toxic adenoma

Front 95

What's the likely cause of hyperthyroidism?
Palpation of multiple thyroid nodules

Back 95

Multinodular goiter

Front 96

What's the likely cause of hyperthyroidism?
Recent study using IV contrast dye (iodine)

Back 96

Hyperthyroidism

Front 97

What's the likely cause of hyperthyroidism?
Eye changes: proptosis, edema, injection

Back 97

Grave’s Disease

Front 98

What's the likely cause of hyperthyroidism?
H/o thyroidectomy or radioablation of thyroid

Back 98

Too much medication

Front 99

What is the next step in the management of a newly-found thyroid nodule in a pt with hyperthyroidism?

Back 99

Check TSH & free T4

Front 100

What is the workup for the underlying cause of DKA?

Back 100

r/o infection (blood cx, urine cx, UA, CXR)
toxicology screen
amylase & lipase
EKG & cardiac enzymes

Front 101

What thyroid abnormalities would you expect to find during pregnancy?

Back 101

↑ TBG & ↑ total T4
normal free T4

Front 102

What is the treatment for proliferative diabetic retinopathy?

Back 102

laser surgery or photocoagulation

Front 103

What is the treatment for peripheral neuropathy?

Back 103

Gabapentin (Neurontin) - analog of the neurotransmitter GABA (doesn’t bind GABA-A or GABA-B receptors, exact MOA unknown)

Pregabalin (Lyrica) – analog of GABA, binds subunit that ↑ Ca2+-dependent release of several NTs

Duloxetine (Cymbalta) – selective serotonin & NE reuptake inhibitor (SNRI), potentiating serotonergic & noradrenergic activity in then CNS

Front 104

What are the 2 most common causes of primary hyperparathyroidism?

Back 104

Parathyroid adenoma
Parathyroid hyperplasia

Front 105

What is the treatment for primary hyperparathyroidism?

Back 105

Surgical parathryoidectomy if one of the following:
Symptomatic (“stones, bones, groans, psychiatric overtone”)
Serum Ca2+ > 1.0 above the upper limit of normal
Creatine clearance reduced by 30%
Bone mineral density scan T-score < -2.5 at any site
Age < 50 yrs
If adenoma & surgery indicated → removal of only the gland contraining the adenoma & biopsy of 1-3 other glands
If hyperplasia & surgery indicated → removal of 3.5 glands and marking the remaining half gland with surgical clip ( or forearm autotransplantation of the gland to remain in cases where recurrence is likely such as MEN type 1)
If surery is not recommended or is refused:
Prevent worsening by hypercalcemia by avoiding thiazides, lithium, volume depletion, prolonged bed rest, or calcium ingestion > 1000mg/day
Adequate hydration (6-8 glasses of water daily) to avoid renal stones
Minimize bone resorption via bisphosphonates, exercise, 1000mg Ca2+ daily (except if calcitriol is elevated) and adequate Vit D intake (400-600 IU/day)
Routine monitoring of
serum Ca2+ (q6mo)
serum Cr (q12mo)
bone density at the hip, lumbar spine and forearm (q12mo)

Front 106

What is the treatment for hyperparathyroidism due to chronic renal disease?

Back 106

Hyperphosphatemia:
Dietary restriction of phosphate (protein)
Oral phosphate binders taken with meals
Calcium carbonate (tums) & acetate (PhosLo) – most commonly used (NOT calcium citrate (Citracal) which ↑ aluminum absorption)
Sevelamer (renagel) nonabsorbable (does not cause hypercalcemia) can be taken with calcium
Lanthanum (fosrenol) long term side effects currently unknown
Aluminum hydroxide (found in Rulox, antacids) – now avoided b/c of gradual induction of aluminum toxicity


Renal osteodystrophy
Lessen hyperphosphatemia via the above measures in order to lessen bone resorption
Calcitriol, other Vit D analog, or cinacalcet (a calcimimetic) to suppress PTH secretion

Front 107

What is a nickname for PTH that aids in remembering its effect on serum phosphate?

Back 107

“Phosphate Trashing Hormone”: it pulls phosphate from the bone and trashes it in the urine - ↑ Ca2+ ↓ phophate ↑ Vit D

Front 108

What are the common causes of primary hyperparathyroidism?

Back 108

Single parathyroid adenoma (85%)
Hyperplasia of the glands (15%)

Front 109

Why might PTH be elevated in renal disease?

Back 109

Can’t activate Vit D to active form in the kidneys

Front 110

What happens to phosphate in pts with hyperparathyroidism caused by renal disease?

Back 110

↑ phosphate

Front 111

What is the disease a/w shortened 4th and 5th digits on the hand “knuckle, knuckle, dimple, dimple”, and what is the derangement?

Back 111

Albright’s hereditary osteodystrophy
Renal unresponsiveness to PTH

Front 112

hypercalcemia + ↑ PTH + ↓ Phosphate

Back 112

Hyperparathyroidism (1° and 3°) – ↑ PTH from adenoma, hyperplasia, MEN1/MEN2A

Familial hypocalciuric hypercalcemia (FHH) inact. mut in Ca sensing receptor in parathyroid & kidney; ↑ Ca2 setpt ±↑ PTH

Front 113

hypercalcemia + ↓ PTH + ↑ Phosphate

Back 113

Vit D excess: intoxication or granulomas (Sarcoid/TB/histo/Wegen) which synthesize 1α-hydroxylase, ↑ 1,25Vit D

Front 114

hypercalcemia + ↓ PTH + ↓ Phosphate

Back 114

Malignancy: ↑ PTHrP [lung SqCC, RCC]
Bone mets – activate osteoclasts ↑ lysis
Multiple myeloma – ↑ IL-1, ↑ bone lysis
*↓PTH = no 1α-hydroxylase= ↓1,25Vit D

Note: ↓ PO4 if PTHrP; nml PO4 if lytic, ↓ 1,25VitD

Milk-alkali syndrome [too much dairy or OD ca-based antacids)

Thiazides [vol depletion ↑ renal reabsorp Ca2+]

Front 115

low calcium, ↑ PTH + ↓ Phosphate

Back 115

Vit D def – can be due to lack of sunlight, malabsorption (celiac dz), Cirrhosis, Drugs (anticonvulsants - phenytoin, rifampin, ketoconazole, F-FU/Leucovorin)


Rickets: Type I absent 1α-hydroxylase (↓ 1,25VitD, tx with Calcitriol) Type 2 absent receptors for Calcitriol, ↑ 1,25Vit D

Front 116

low calcium, ↑ PTH + ↑ Phosphate

Back 116

Pseudohypoparathyroidism: Aut Dom, end-organ resistance to PTH
(including ↓ 1α-hydroxylase)


Chronic Renal failure (2° hyperpara) –
↓ 1,25VitD, ↑ PO4 from ↓ clearance

Front 117

low calcium, low PTH, high phosphate

Back 117

HypOparathyroidism: sporadic, or iatrogenic (s/p thyroid surgery, neck radiation) Wilson’s, hemochromatosis,

hypoMg (Mg cofactor for adenylate cyclase, cAMP required for PTH activat)

Front 118

what are the pitfalls in measuring calcium?

Back 118

Physiologically active Ca2+ is free (ionized)
Serum Ca2+ reflects total Ca2+ (bound + unbound) and ∴ influenced by albumin (main Ca2+ binding protein)
Corrected Ca2+ = measured Ca2+ + [0.8 x (4 – albumin)]
Alkalosis will cause more Ca2+ to be bound to albumin → therefore total Ca2+ may be normal, but ↓ ionized Ca2+
Best to measure ionized Ca2+ directly

Front 119

Signs/ Symptoms of hypercalcemia in hyperparathyroidism?

Back 119

“STONES”:
renal stones
nephrocalcinosis: polyuria, polydipsia, uremia
“BONES”: ↑ osteoclastic activity
osteitis fibrosa cystica: rare today b/c of early detection commonly involves the jaw/ fingers, histologically the pathognomonic features are ↑ osteoclasts on surface of the bone & replacement of normal cellular & marrow elements with fibrous tissue – xrays show periosteal resorption
osteoporosis
osteomalacia
osteoarthritis
“GROANS”: GI manifestations:
constipation, nausea, vomiting
peptic ulcers
pancreatitis
“PSYCHIATRIC OVERTONES”:
Lethargy, fatigue, depression
Memory loss
Psychosis
Personality changes
Confusion, stupor, coma
Other:
Proximal muscle weakness, keratitis, conjunctivitis, HTN, itching

Front 120

What are the symptoms of hyperprolactinemia? (high yield!)

Back 120

Premenopausal female → Hypogonadism
Infertility, Oligo- or amenorrhea
Rarely galactorrhea
Post-menopausal → Already hypogonadal, less symptoms, +/- galatorrhea
Male: ↓ testosterone: ↓ libido, impotence, ↓ sperm ct (infertility), gynecomastia
+/- galactorrhea

Front 121

Whats the workup if you suspect a prolactinoma?

Back 121

Prolactin levels
TSH
MRI of brain

Front 122

What is the treatment for a prolactinoma?

Back 122

First step: Dopamine agonist – Cabergoline (Dostinex) > bromocroptine or pergolide
If Dopamine agonist ineffective → switch to a 2nd agonist
If 2 dopamine agents are ineffective → Transphenoidal surgery
If female with adenoma >3cm and desire to become pregnant (during which time the dopamine agonist is withheld) → transphenoidal surgery even if the dopamine agonist is effective
If large adenoma is surgically removed → radiation therapy after surgical debulking

Front 123

What are the S/S of acromegaly? What tests can be used to confirm the diagnosis?

Back 123

Note: the average time from onset to diagnosis is 12yrs and it presents with the following symptoms:
Enlarged jaw (teeth spread apart), nose & frontal bones (coarse facial features), hand & feets (increase in ring, glove, shoe size)
Soft tissue growth: voice deepens, macroglossia (teeth indentations in tongue), carpal tunnel syndrome and other entrapment syndromes, hypertrophy of synovial tissue and cartilage → arthropathy
cardiovascular disease: HTN, LVH, diastolic dysfxn
Glucose intolerance in 50%, DM in 10%
Diagnostic testing:
Screening: measure serum levels of insulin-like growth factor 1 (IGF-1)
Confirm diagnosis: with oral glucose suppression test (75g glucose → measure GH at 1 hr and 2hr → if GH conc is > 1ng/mL = acromegaly)
If testing positive for acromegaly → pituitary MRI to eval for mass or empty sella

Front 124

What is the treatment for acromegaly?

Back 124

Transphenoidal resection of pituitary adenoma or external beam radiation
If unable to resect adenoma → somatostatin analog – Octreotide (Sandostatin) or lanreotide (Somatuline) – inhibits GH secretion
If somatostatin analog ineffective → cabergoline (dopamine agonist that inhibits GH secretion)
Bromocriptine is less effective than is cabergoline
if cabergoline ineffective → pegvisomant (GH receptor antagonist)

Front 125

What is the usual presentation of Sheehan syndrome? (HYQ!)

Back 125

Postpartum hemorrhage → hypotension → infarction of the pituitary gland → hypopituitarism
Severe Sheehan → first few days-weeks after delivery → lethargy, anorexia, weight loss, and inability to lactate
mid Sheehan → wks, months, or yrs after delivery → mild fatigue, anorexia, weight loss; failure of postpartum lactation, failure to resume menses, and loss of sexual hair
possible ACTH deficiency → hypocortisolism
Possible TSH deficiency → hypothyroidism

Front 126

Which 2 hormone levels are decreased in response to excess prolactin?

Back 126

↓ LH & ↓ FSH (leads to hypogonadal symptoms of infertility, gynecomastia, galatorrhea)

Front 127

What common medications can cause hyperprolactinemia?

Back 127

Medications that antagonize dopamine
Neuroleptics (Risperidone)
Domperidone
Metoclopramide
Methyldopa

Front 128

What is the visual field defect classically assoc with prolactinoma?

Back 128

Bilateral hemianopsia (mass effect of tumor in sella turcica)

Front 129

What are the first-line drugs used to treat prolactinomas?

Back 129

Dopamine agonists (Cabergoline > bromocriptine, pergolide)

Front 130

What substance is used in screening for acromegaly? What study is used to confirm the diagnosis?

Back 130

Screening: measure serum IGF-1 (can’t measure GH b/c it varies during the day)
Confirmatory: oral glucose suppression test
Give 75g glucose → measure GH at 1 hr and 2hr → if GH conc is > 1ng/mL = acromegaly

Front 131

What complications can result from acromegaly?

Back 131

Cardiac failure
Diabetes
Spinal cord compression
Compression of optic nerve → vision loss

Front 132

What is Sheehan syndrome?

Back 132

Postpartum hemorrhage → pituitary infarction → pituitary dysfunction

Front 133

What changes in serum potassium (K+) & serum sodium (Na+) would be seen in patients with excessive aldosterone [Conn’s Syndrome] or adrenal insufficiency [Addison’s Disease]?

Back 133

Addison’s is due to Adrenal Atrophy and Absence of hormone production
Conn’s is HYPERaldosteronism due to an aldosterone-secreting tumor → muscular weakness, hypertension, hypokalemia, alkalosis- Conn’s are “HYPER”-aldosterone, but muscles are really weak
Conn’s Syndrome: HypOkalemia, HYPERnatremia
Addison’s Disease: HYPERkalemia, HypOnatremia

Front 134

What mineralcorticoid medication is used to tx pts with hypoaldosteronemia [Addison’s Disease] ?

Back 134

Fludrocortisone (Florinef)

Front 135

What aldosterone antagonist can be given to treat HYPERaldosteronemia? What effect would this drug have on serum K+ levels?

Back 135

Spironolactone (Aldactone): would ↑ serum K+

Front 136

What condition(s) do you see ↑ aldosterone : ↓ renin?

Back 136

Primary Hyperaldosteronism:
Conn’s syndrome (adrenal adenoma secreting aldosterone)

Front 137

What condition(s) do you see ↑ aldosterone : ↑ renin?

Back 137

Secondary Hyperaldosteronism:
Renovascular disease,
Renin-secreting tumor
CHF, cirrhosis, nephrotic syndrome
Hypovolemia, diuretic use

Front 138

What condition(s) do you see ↓ aldosterone : ↓ renin?

Back 138

Non-aldosterone mineralcorticoid excess:
Cushing’s syndrome (see below)
Chronic licorice ingestion

Front 139

What are some causes of Cushing’s syndrome?

Back 139

Excess corticosteroid administration (most common)
Pituitary adenoma (Cushing’s disease) – producing ACTH
Paraneoplastic ACTH production – small cell lung cancer
Adrenal tumor – producing cortisol

Front 140

What can a high dose of dexamethasone suppress? What can it not suppress?

Back 140

If am cortisol suppressed → pituitary adenoma producing ACTH (Cushing’s disease)
If am cortisol not suppressed → adrenal tumor producing cortisol, or ectopic ACTH secreting tumor (small cell lung ca)

Front 141

What are the electrolyte abnormalities found in hyperaldosteronism?

Back 141

hypOkalemia, HTN, metabolic alkalosis (↓ K+, mildy ↑ Na+)

Front 142

A pt with a high plasma aldosterone concentration and low plasma renin activity ratio has what condition? Which medication could be used to treat this condition until definitive therapy can be undertaken?

Back 142

Dx: Conn’s Syndrome
Tx: Spironolactone (Aldactone)

Front 143

Increased skin pigmentation is seen in pts with which kind of adrenal insufficiency?

Back 143

Dx: Addison’s disease = Primary adrenal insufficiency
Pathophys: autoimmune destruction of adrenal cortex

Front 144

Which steroid is used to replace mineralcorticoid deficiency?

Back 144

Fludrocortisone (Florinef)

Front 145

A pt on chronic steroid therapy contracts pneumonia that requires admission into the ICU. What should the admitting physician make sure to do with the pt’s medications and why?

Back 145

Increase the dose of steroids
(during times of stress, adrenals tend to ↓ activity)

Front 146

What is the likely condition of a female infant with virilization of the genitalia and hypotension?

Back 146

Congenital adrenal hyperplasia → 21-α hydroxylase def

Front 147

What serum lab abnormality would you see in a 17-α hydroxylase def and in 21-α hydroxylase deficiency?

Back 147

17-α: hypOkalemia, mildly ↑ Na+, HTN
21-α: hypOnatremia, hyperkalemia, hypotension

Front 148

A 23 yo F presents with c/o episodic anxiety, palpitations, and sweating. She managed to measure her BP during one of the episodes which revealed 165/103, a large increase over her normal 118/77. What tests should be ordered to aid in diagnosis of her condition?

Back 148

Dx: Pheochromocytoma
Labs: urinary catecholamines, metanephrines & vanillylmadelic acid (VMA), plasma free metanephrines

Front 149

What is the medical management of the above pt’s condition prior to her having the necessary surgery for a definitive cure?

Back 149

Tx: α-blockade before β-blockers

Front 150

A pt with acromegaly is found to have elevated Ca2+ on a blood draw during a work up of his peptic ulcer disease. What is the diagnosis of this pt?

Back 150

Dx: MEN 1 syndrome
Acromegaly, ↑ Ca2+ from hyperparathyroidism, peptic ulcer disease (Zollinger-Ellison syndrome)

Front 151

What tumors are associated with MEN 2a?

Back 151

Medullary thyroid cancer
Hyperparathyroidism
Pheochromocytoma

Front 152

HYQ: A pt with ↑BP, palpitations, HA, excessive perspiration is found to have elevated urine vanillymandelic acid levels. What effect would giving a β-blocker have on this pt?

Back 152

Dx: Pheochromocytoma
Giving β-blockers will rapidly raise the blood pressure more

Front 153

HYQ: What is lactotroph adenoma? What is a somatotroph adenoma?

Back 153

Lactotroph adenoma: Prolactin secreting
Somatotroph adenoma: GH secreting

Front 154

HYQ: Most likely cause of ↑ PTH + ↓ serum Ca2+ + ↑ serum phosphate?

Back 154

Renal failure with Vit D Deficiency

Front 155

HYQ: Of DHEA, DHEA-S, and testosterone, which is made only by the adrenal and is more specific marker for an androgen-producing adrenal tumor in a woman?

Back 155

DHEA-sulfate

Front 156

HYQ: What is the most specific lab finding in making the diagnosis of primary hyperaldosteronism?

Back 156

High PAC: PRC ratio

Front 157

What is the next step in the management of a pt with hyperprolactinemia not due to an obvious drug cause?

Back 157

MRI of the brain (sella turcica)
Check TSH

Front 158

What is the next step in the management of a pt found to have an absent pituitary on MRI (empty sella)?

Back 158

Reassurance if not symptomatic

Front 159

What drugs are known for causing ↑prolactin levels?

Back 159

Phenothiazine, thioridazine, prochlorperazine, promethazine
Other antipsychotics (Risperidone, haloperidol)
Methyldopa
Verapamil

Front 160

What are the indications for surgical parathyroidectomy?

Back 160

Symptomatic
Serum Ca2+ conc >1.0 mg/dL above the upper limit of normal
24hr urine Ca2+ > 400mg
Cr Clearance reduced by 30%
Bone mineral density T-score < -2.5 at any site
Age < 50 yrs

Front 161

(H/P) = rhinorrhea (i.e., nasal congestion & increased secretions), nonproductive cough; nasal and throat irritation, sneezing, possible fever, no exudates or productive coughLabs = negative throat culture

Back 161

Upper respiratory infections (URI)Inflammation of the upper airways most commonly caused by rhinovirus, coronavirus, or adenovirus

Hint 161

Treatment = rest, analgesia, treat symptoms; antibiotics are NOT helpful

Front 162

H/P = sore throat, tonsillar exudates (more common w/ bacterial infection), lymphadenopathy, possible nasal congestion; fever, red and swollen pharynx,

Back 162

PharyngitisPharyngeal infection caused by group A β-hemolytic streptococci (“strep throat”) or common cold virusComplications = untreated infection can cause rheumatic heart disease or glomerulonephritis (characterized by a high antistreptolysin O titer)

Hint 162

Labs = throat culture grows streptococcal species, and rapid streptococcal Ag test is + for strep throat; - culture suggests viral etiologyTreatment = self-limited; β-lactam antibiotics (e.g., penicillin, amoxicillin, etc.) reduce infection time

Front 163

H/P = similar to streptococcal pharyngitis, tonsillar exudates; ear pain, difficulty swallowing; possible high fever.

Back 163

Tonsillar infectionsSpread of streptococcal pharyngitis to palatine tonsils leading to tonsillar inflammation (i.e., tonsillitis)Complications = airway compromise; abscess (requires intravenous [IV] antibiotics and surgical incision and drainage followed by tonsillectomy after resolution to prevent recurrence)

Hint 163

Treatment = self-limited; β-lactam antibiotics (e.g., penicillin, amoxicillin, etc.) reduce infection time

Front 164

H/P = myalgias, vomiting, diarrhea; high fevers (typically >100°F/37.8°C and can reach up to 106°F/41°C), arthralgias, sore throat, nasal congestion, nonproductive cough, nausea, lymphadenopathy

Back 164

Viral influenzaGeneralized infection with URI symptoms caused by one of several influenza viruses

Hint 164

Labs = serologic tests are definitive, but rarely required for diagnosisTreatment = treat symptoms; fluid intake important to replace losses from vomiting and diarrhea; self-limited (several days) but amantadine may shorten course of disease; elderly patients, health care workers, immunocompromised patients, and patients with lung disease should receive annual vaccine to reduce risk of infection

Front 165

pain over infected sinuses, purulent nasal discharge, maxillary toothache pain; pain on palpation of affected sinuses, illumination test (i.e., light held close to sinuses) may detect congestion in frontal of maxillary sinuses, but is unreliable

Back 165

SinusitisSinus (most maxillary)infection associated w/ allergic rhinitis, barotrauma, viral infection, prolonged nasogastric tube placement, or asthmaAcute sinusitis is usually caused by Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, viral infectionAcute sinusitis can spread to CNS & cause meningitis if untreated.Chronic sinusitis (lasting >3 months) is usually caused by sinus obstruction, anaerobic infection; patients with diabetes mellitus (DM) predisposed to mucormycosis

Hint 165

Radiology = radiograph shows opacification and fluid levels in affected sinuses; computed tomography (CT) is diagnostic; frequently radiologic tests are not needed because of clinical diagnosisTreatment = treat symptoms; amoxicillin × 2 weeks in acute cases and for 6–12 weeks in chronic cases; surgical drainage or correction of anatomic obstruction may be required for full cure

Front 166

H/P = productive cough, sore throat; fever, wheezing, tight breath sounds

Back 166

Acute bronchitis Inflammation of trachea and bronchi caused by spread of URI or exposure to inhaled irritants

Hint 166

Labs = sputum culture only performed in persistent cases and is most commonly -;Radiology = chest x-ray (CXR) may show only mild congestionTreatment = self-limited if viral (most cases); patient groups with an increased risk of bacterial infection (e.g., smokers, elderly, patients with other lung disease) may be given antibiotics (e.g., fluoroquinolones, tetracycline, or erythromycin)

Front 167

H/P = pleuritic chest pain; decreased breath sounds, dullness to percussion, tachypnea, productive or nonproductive cough, dyspnea, chills, night sweats, rales, wheezing, egophony (i.e., change in voice quality heard during auscultation over a consolidated region of lung), tactile fremitusLabs = increased white blood cell count (WBC) (slight increase with viral cause, significant increase with bacterial or fungal cause) with left shift (more immature forms); + sputum culture

Back 167

PneumoniaInfection of the bronchoalveolar tree can be caused by common nasopharyngeal bacteria (i.e., typical pneumonia) or bacteria, viruses, or fungi from the surrounding environment (i.e., atypical pneumonia); common causes vary by age group

Hint 167

Treatment = viral pneumonia is self-limited and only requires supportive care; bacterial and fungal pneumonias require antibiotics (started as broad coverage and changed to pathogen-specific therapy as culture results become availableAdmission=elderly, multiple medical comorbidity, significant laboratory abnormalities, multilobar involvement, signs of sepsis

Front 168

H/P=a non-productive cough be used for influenza A virus

Back 168

Viral Pneumonia Viral (influenza, parainfluenza, adenovirus, cytomegalovirus, respiratory syncytial virus) Most common pneumonia in children; common in adults

Hint 168

Treatment=Self-limited; amantidine may

Front 169

H/P=pneumonia, high fevers, pleuritic pain, productive cough

Back 169

Streptococcus pneumoniae Most common pneumonia in adults; higher risk of infection in sickle cell patients

Hint 169

Treatment=β-lactams, macrolides(azithromycin, clarithromycin, erythromycin)

Front 170

H/P=pneumonia, slower onsetPatients with COPD; higher risk of infection in patients with sickle cell disease

Back 170

Haemophilus influenzae

Hint 170

Treatment=β-lactams, TMP-SMX

Front 171

H/P=pneumonia, abscess formationNosocomial pneumonia, immunocompromised patients

Back 171

Staphylococcus aureus

Hint 171

Treatment=β-lactams

Front 172

H/P=pneumonia, “Currant-jelly” sputum; Alcoholics, patients with high risk of aspiration, patients staying in the hospital for extended amounts of time, sickle cell patients

Back 172

Klebsiella pneumoniae

Hint 172

Treatment=Both cephalosporins and aminoglycosides (gentamicin, tobramycin)

Front 173

H/P=pneumonia, Young adults, possible rash; + cold-agglutinin test

Back 173

Mycoplasma pneumoniae

Hint 173

Treatment=Macrolides (azithromycin, clarithromycin, erythromycin)

Front 174

H/P=pneumonia, rapid onsetChronically ill and immunocompromised patients, patients with cystic fibrosis, nosocomial pneumonia

Back 174

Pseudomonas aeruginosa

Hint 174

Treatment=Fluoroquinolones (ciprofloxacin), aminoglycosides, generation 3rd-cephalosporins

Front 175

H/P=pneumonia Slow onset, nausea, diarrhea, confusion, or ataxia

Back 175

Legionella pneumophilaAssociated with aerosolized water (air-conditioners)

Hint 175

Treatment=Macrolides, fluoroquinolones

Front 176

H/P=pneumonia, Slow onset, frequent sinusitisMore common in very young and elderly

Back 176

Chlamydia pneumoniae

Hint 176

Treatment=Doxycycline, macrolides

Front 177

H/P=pneumonia, Respiratory distress, lethargyNeonates and infants

Back 177

Group B Streptococcus

Hint 177

Treatment=β-lactams

Front 178

H/P=pneumoniaNosocomial pneumonia, elderly patients

Back 178

Enterobacter sp.

Hint 178

Treatment=TMP-SMX

Front 179

H/P=pneumonia, Less severe symptoms; subacute disease for initial history

Back 179

FungiTravelers to southwest U.S. (coccidioidomycosis), caves (histoplasmosis), or Central America (blastomycosis)

Hint 179

Treatment=Antifungal agents (amphotericin B, ketoconazole)

Front 180

H/P=pneumonia, Slow onset, GI symptomsImmunocompromised patients (HIV) (CD4 count <200)

Back 180

Pneumocystis carinii (fungi-like)

Hint 180

Treatment=TMP-SMX

Front 181

H/P = cough, hemoptysis, dyspnea, weight loss, night sweats; fever, ralesRisk factors = immunosuppression, alcoholism, lung disease, DM, advanced age, homelessness, malnourishment, crowded living conditions, and close proximity to infected patientsRadiology = CXR may show apical fibronodular infiltrates (reactivated disease), lower-lobe infiltrates (primary lesion), and calcified granulomas/lymph nodes (Ghon complexes)

Back 181

Tuberculosis (TB)Pulmonary infection caused by Mycobacterium tuberculosisFollowing primary infection, disease enters inactive state; untreated infections can become reactivated (most active cases) and extend to extrapulmonary sites (i.e., miliary TB)

Hint 181

Labs = + purified protein derivative (PPD) tuberculin skin test is screening test for exposure (followed by a CXR to look for signs of TB), anergy test (subcutaneous Candida preparation) in addition to a PPD to check for an appropriate immune response; + sputum acid-fast stain, + culture (may take weeks, so not useful in planning therapy); 1 bronchoscopy is considered equal to 3 sputum samples for specimen collectionTreatment = respiratory isolation for any inpatient; report all diagnosed cases to local and state health agencies; multidrug treatment initially w/ isoniazid (INH), rifampin, pyrazinamide, & ethambutol followed by INH & rifampin for a total of 6 months; give vitamin B6 w/ INH to prevent peripheral neuritis (INH competes with vitamin B6 as a cofactor in neurotransmitter synthesis, so supplemental vitamin B6 helps offset this competition); give prophylactic INH to patients with an asymptomatic positive PPD who are immunocompromised, have a history of IV drug abuse (IVDA), are <35 years of age, a history of close contact with TB-infected people, or are indigent patients (reporting is unnecessary unless TB is diagnosed); monthly sputum acid-fast tests should be performed during therapy to confirm adequate treatment

Front 182

H/P = acute dyspnea and pulmonary decompensation in setting of serious underlying condition; cyanosis, tachypnea (begins within 48 hours of initial insult), wheezing, rales, rhonchiLabs = arterial blood gas (ABG) shows respiratory alkalosis, decreased O2 (caused by impairment of O2 transfer to pulmonary capillaries by pulmonary edema), decreased CO2 (caused by hyperventilation); other tests should reflect underlying pathology; Swan-Ganz catheterization shows wedge pressure <18 mm Hg; Pao2:Fio2 ratio will be <200 during mechanical ventilation

Back 182

Acute respiratory distress syndrome (ARDS)Acute respiratory failure caused by sepsis, trauma, aspiration, near drowning, drug overdose, shock, or lung infection that is characterized by refractory hypoxemia, decreased lung compliance, and pulmonary edema, and carries a high mortalityEtiology=ARDS: Aspiration/Acute pancreatitis/Air or Amniotic embolism, Radiation, Drug overdose/Diffuse lung disease/DIC/Drowning, Shock/Sepsis/Smoke inhalation.

Hint 182

Radiology = bilateral pulmonary edema and infiltratesTreatment = treatment in intensive care unit with mechanical ventilation frequently required; mechanical ventilation should include positive end-expiratory pressure (PEEP), increased inspiratory times, and Fio2 adjusted to maintain O2 saturation (Sao2) >90%; underlying cause must be treated; keep fluid volumes low to prevent pulmonary edema; use of extracorporeal membrane oxygenation (ECMO) may improve outcome in severe cases

Front 183

H/P = prolonged expiratory duration, accessory muscle use, cough, dyspnea, wheezing, chest tightness; tachypnea, tachycardia, decreased breath sounds, wheezing, possible pulsus paradoxus; cyanosis, decreased arterial O2 saturation (Sao2) on pulse oximetry, or difficulty talking in severe attacks

Back 183

AsthmaReversible airway obstruction secondary to bronchial hyperactivity, acute airway inflammation, mucous plugging, and smooth muscle hypertrophyExacerbations (i.e., sudden bronchoconstriction and airway inflammation) are triggered by allergens (e.g., dust, smoke, pollen, fumes, pet dander), URI, exercise, stress, β-antagonist drugs, aspirin (rare), and sulfites (rare)Risk factors = family history of asthma, allergies, atopic dermatitis, low socioeconomic statusDisease can be worse in childhood and improve with age

Hint 183

Labs = peak expiratory flow rate (PEFR) decreased and used along with clinical symptoms and frequency of medication use to classify disease as mild intermittent, mild persistent, moderate persistent, or severe (see Table 2-8); PFT show decreased FEV1, normal/elevated DLcoRadiology = CXR shows hyperinflationTreatment=Inhaled short-acting β2-agonist IV corticosteroids if persistent during exacerbation. daily corticosteroid inhaler (+long long-acting β2-agonist, considerleukotriene inhibitor or theophylline) from Mild Persisent up

Front 184

prolonged, nonresponsive asthma attack

Back 184

Status asthmaticus

Hint 184

Treatment=aggressive bronchodilator therapy, corticosteroids, O2, and, possibly, intubation

Front 185

H/P = productive cough, recurrent respiratory infections, dyspnea; wheezing, rhonchihistory of productive cough for 3 months of the year for >2 years

Back 185

Chronic bronchitisChronic bronchial inflammation associated with tobacco use (common) or chronic asthma (uncommon); occurs in continuum with emphysema as chronic obstructive pulmonary disease (COPD)“blue bloaters,” because secondary development of cor pulmonale causes cyanosis and peripheral edema;Complications = emphysema frequently results without smoking cessation

Hint 185

Labs = PFTs show gradually worsening signs of obstructive disease as condition progressesTreatment = tobacco cessation, antibiotics given for URI because of the greater incidence of a bacterial etiology; bronchodilators during exacerbations

Front 186

H/P = dyspnea, possible productive cough, morning headache; barrel-chested, pursed-lip breathing, prolonged expiratory duration, decreased heart sounds, decreased breath sounds, wheezing, rhonchi, accessory muscle use, jugular venous distension (JVD); exacerbations present with worsening symptoms

Back 186

Emphysema (later stage—COPD)Long-term tobacco use leads to chronic bronchoalveolar inflammation associated with release of proteolytic enzymes by neutrophils and macrophages; destruction of alveoli and bronchioles results with panacinar airspace enlargement and a decreased capillary bedLess common form (appears at younger age) caused by α1-antitrypsin deficiencycommon form of emphysema has a centrilobular distribution, whereas the form associated with α1-antitrypsin deficiency has a panlobular distribution.

Hint 186

Labs = PFTs show decreased FEV1, decreased FEV1/FVC, increased total lung capacity (TLC), decreased PEFR; ABG during acute exacerbations shows decreased O2, increased CO2 (beyond a baseline increase already seen in these patients)Radiology = CXR shows flat diaphragm, hyperinflated lungs, subpleural blebs and bullae (i.e., small fluid-filled sacs), and decreased vascular markingsTreatment = smoking cessation; supplemental O2; inhaled, short-acting β2-agonists; inhaled anticholinergics; inhaled corticosteroids and long-acting β2-agonists may be useful in severe cases; antibiotics given for respiratory infections; pneumococcal and influenza vaccines important to reduce infection risk; enzyme replacement may have a role in α1-antitrypsin deficiency therapy; lung transplant may be an option in late severe disease

Front 187

H/P = copious sputum, persistent, productive cough; hemoptysis, frequent respiratory infections, dyspnea; wheezing, rales, and hypoxemia

Back 187

D. BronchiectasisPermanent dilation of small and medium bronchi because of destruction of bronchial elastic componentsOccurs secondary to chronic airway obstruction, chronic tobacco use, TB, fungal infections, severe pneumonia, or cystic fibrosisComplications = cor pulmonale, massive hemoptysis, abscess formation

Hint 187

Radiology = multiple cysts and bronchial crowding seen on CXR; CT shows dilation of bronchi, bronchial wall thickening, bronchial wall cystsTreatment = pulmonary hygiene (e.g., hydration, sputum removal), chest physical therapy; antibiotics given when sputum production increases; inhaled β2-agonists and corticosteroids may reduce symptoms; resection of severely diseased regions of lung indicated for hemorrhage, substantial sputum production, or inviability

Front 188

H/P = possibly asymptomatic; hemoptysis, cough, dyspnea, pleuritic chest pain, fatigue, weight loss, frequent pulmonary infections;

Back 188

Lung cancerMost frequently associated with tobacco use (~90% of cases); also can be caused by occupational exposures (e.g., smoke, asbestos)Complications = poor prognosis (~10% 5-yr survival); recurrence common for primary tumors

Hint 188

Radiology = initially seen on CXR or CT as pulmonary nodule; bronchoscopy with biopsy and brushings or fine needle aspiration of lesion are diagnosticTreatment = use of surgical resection, chemotherapy, and/or radiation therapy based on type of lung cancer (large cell, squamous cell, or adenocarcinoma vs. small cell) and staging of disease (based on local extension, lymph node involvement, and presence of metastases) (see Table 2-11)

Front 189

miosis, ptosis, and anhidrosis

Back 189

Horner's syndrome

Front 190

Horner's syndrome plus brachial plexus involvement

Back 190

Pancoast's syndrome

Front 191

obstruction of venous drainage through superior vena cava and associated head swelling and CNS symptoms

Back 191

Superior vena cava syndrome

Front 192

Lung Cancer, CentralCavitary lesions; direct extension to hilar lymph nodesParaneoplastic Syndromes= Hypercalcemia, Dermatomyositis

Back 192

Squamous cell carcinoma

Hint 192

Treatment=Chemotherapy as primary, Radiation Therapy as adjuvant

Front 193

Lung Cancer,PeripheralWide metastases; can be caused by asbestos; pleural effusions show increased hyaluronidase levels; bronchiolar cancer is subtype that is low grade and occurs in single nodulesParaneoplastic Syndromes= DIC, Thrombophlebitis,, Microangiopathic hemolytic anemiaDermatomyositis

Back 193

Adenocarcinoma

Hint 193

Treatment for all non-small:no lymph node involvement beyond ipsilateral hilar nodes, No mediastinal invasion, no metastases->Surgical resection, radiation as primary or postop adjuvant, chemo as adjuvant

Front 194

Lung Cancer, CentralRapidly growing; early distant metastases; several paraneoplastic syndromesParaneoplastic Syndromes= Cushing's syndrome, Syndrome of inappropriate ADH secretion (SIADH), Ectopic growth hormone and ACTH secretion, Peripheral neuropathy, Subacute cerebellar degeneration, Eaton-Lambert syndrome (similar presentation to myasthenia gravis), Subacute sensory neuropathy, Limbic encephalitis, Dermatomyositis

Back 194

Small cell carcinoma

Hint 194

Treatment for all non-small:has extension to ipsilateral mediastinal nodes, No mediastinal invasion or metastases->radiation as primary, surgery if tumor shrinik, chemo as induction for surgery or adjuvant

Front 195

Lung Cancer, PeripheralLate distant metastases, early cavitationParaneoplastic Syndromes=Gynecomastia, Dermatomyositis

Back 195

Large cell carcinoma

Hint 195

Treatment for all non-small:Mediastinal invasion, distant nodes, and/or metastases-> chemo or radiation as palliative

Front 196

H/P = hoarseness that worsens with time (over several weeks), dysphagia, ear pain, hemoptysis; laryngoscopy may visualize mass and airway obstruction

Back 196

Laryngeal cancerSquamous cell cancer of the larynx associated with tobacco and alcohol use

Hint 196

Labs = biopsy is diagnosticRadiology = magnetic resonance imaging (MRI) or CT with contrast detects soft tissue mass; PET may be useful for detecting lesions earlier in disease courseTreatment = partial or total laryngectomy used to remove lesions confined to larynx; radiation therapy can be used in conjunction with surgery or as sole therapy in extensive lesions; advanced cases may require combination of surgery, radiation, and chemotherapy to resect lesion while preserving surrounding structures

Front 197

H/P = progressive exercise intolerance, dyspnea; dry crackles, JVD, tachypnea, and possible digital clubbingpatients >50 years of ageLabs = PFT will show restrictive lung disease characteristics (e.g., FEV1/FVC normal, decreased FVC, decreased TLC, decreased compliance); bronchioalveolar lavage shows increased polymorphonuclear (PMN) cells; lung biopsy demonstrates extensive fibrosis and loss of parenchymal architectureRadiology = CXR shows reticulonodular pattern and “honeycomb” lung in advanced cases; CT will show lung fields with “ground glass” appearance

Back 197

Idiopathic pulmonary fibrosis (IPF)Inflammatory lung disease causing lung fibrosis;Complications = progressive lung fibrosis with frequent mortality within 5 years; most patients do not survive sufficiently long to receive a lung transplant

Hint 197

Treatment = corticosteroids combined with either azathioprine or cyclophosphamide are helpful in some patients (follow PFTs to evaluate effectiveness); worsening PFTs should indicate need to change drug regimen; lung transplant is frequently indicated

Front 198

H/P = cough, malaise, weight loss, dyspnea, arthritis (knees, ankles), chest pain; fever, erythema nodosum (i.e., tender red nodules on shins and arms), lymphadenopathy, vision loss, cranial nerve palsiesLabs = increased serum angiotensin-converting enzyme (ACE), increased calcium, hypercalciuria, increased alkaline phosphatase, decreased WBC, increased erythrocyte sedimentation rate (ESR); PFT show decreased FVC, decreased DLcoRadiology = CXR shows bilateral hilar lymphadenopathy, pulmonary infiltrates (ground glass appearance)

Back 198

SarcoidosisSystemic disease characterized by noncaseating granulomas, hilar adenopathy, pulmonary infiltrates, and skin lesions; unknown etiologyRisk factors = blacks > whites; females > males; most frequently occurs between 10 and 40 years of agePatients with sarcoidosis frequently show anergy (no reaction) to a skin test or PPD.

Hint 198

Treatment = occasionally self-resolving; corticosteroids in chronic cases; cytotoxic drugs can be used with failure of steroid therapy; lung transplantation is rarely required (only in severe cases)

Front 199

H/P = symptoms begin when significant pulmonary fibrosis has occurred (several years between exposure to onset of symptoms is common); cough, dyspnea on exertion, heavy sputum production; rales and wheezing are heard on auscultation, digital clubbing

Back 199

PneumoconiosesInterstitial lung diseases that result from long-term occupational exposure to substances that cause pulmonary inflammation

Hint 199

Labs = PFT show a restrictive patternRadiology = CXR shows multinodular opacities; CT shows signs of pulmonary fibrosisTreatment = usually, no successful treatments are available for these conditions; prevention (e.g., proper air filters, following safe-handling recommendations) is vital to avoiding disease

Front 200

H/P = hemoptysis, dyspnea, recent respiratory infectionLabs = + anti-GBM Ab; PFT show restrictive pattern, but increased DLco (caused by the presence of Hgb in alveoli); urinalysis shows proteinuria and granular casts; renal biopsy shows crescentic glomerulonephritis and IgG deposition along glomerular capillaries

Back 200

Goodpasture's syndromeProgressive autoimmune disease of lungs and kidneys caused by anti-glomerular basement membrane (anti-GBM) antibodies and characterized by intra-alveolar hemorrhage and glomerulonephritis

Hint 200

Radiology = CXR shows bilateral alveolar infiltrationTreatment = plasmapheresis to remove auto-antibodies; corticosteroids and immunosuppressive agents

Front 201

H/P = ulcerations of nasopharynx, fever; hemoptysis, dyspnea, myalgias, chronic sinusitis; additional symptoms from renal (e.g., mild hematuria), CNS (e.g., hearing loss, sensory neuropathy, cranial nerve dysfunction), ophthalmologic (e.g., conjunctivitis, proptosis, corneal ulceration, diplopia), and cardiac (e.g., arrhythmia) involvementLabs = + cytoplasmic antineutrophil cytoplasmic antibody (c-ANCA); biopsy shows noncaseating granulomas; renal biopsy detects vasculitic process

Back 201

Wegener granulomatosisRare disease with granulomatous inflammation and necrosis of lung and other organ systemsCaused by systemic vasculitis that mainly affects lung and kidney causing formation of noncaseating granulomas and destruction of lung parenchymaComplications = rapidly fatal if untreated

Hint 201

Treatment = cytotoxic therapy (e.g., cyclophosphamide), corticosteroids

Front 202

PneumoconiosesWorking with insulation, construction, demolition, building maintenance, automobiles

Back 202

AsbestosisComplications=Increased risk of malignant mesothelioma and lung cancer; synergistic effect with tobacco

Hint 202

Labs=pleural biopsy show asbestos fibersRadiology= Multinodular opacities, pleural effusions, blurring of heart/diaphragm; chest CT shows linear pleural/parenchymal fibrosis

Front 203

PneumoconiosesMining, pottery making, sandblasting, cutting granite

Back 203

SilicosisComplications=Increase risk of TB infection; progressive fibrosis

Hint 203

Radiology=Small apical nodular opacities; hilar adenopathy

Front 204

Pneumoconioses.Coal mining

Back 204

Coal worker's diseaseComplications=Progressive fibrosis

Hint 204

Radiology=Small apical nodular opacities

Front 205

PneumoconiosesElectronics, ceramics, tool, die manufacturing

Back 205

BerylliosisComplications=Increased risk of lung cancer;

Hint 205

Labs=Pulmonary edema, diffuse granuloma formationRadiology=Diffuse infiltrates; hilar adenopathyTreatment=may need chronic corticosteroid treatment to maintain respiratory function

Front 206

H/P = sudden dyspnea, pleuritic chest pain, cough, syncope, hemoptysis, feeling of impending doom; fever, tachypnea, tachycardia, cyanosis, loud S2, decreased breath sounds over regions of effusionLabs = increased A-a gradient; increased D-dimer; ABG shows increased CO2, decreased O2 (<80 mm Hg), ventilation-perfusion scan (V/Q scan) may show areas of mismatchECG = tachycardia, may show S wave in lead I and T-wave inversion in lead V3

Back 206

Pulmonary embolism (PE)Occlusion of pulmonary vasculature by a dislodged thrombusIncreasing pulmonary artery pressure caused by occlusion leads to right-sided heart failure, hypoxia, and pulmonary infarctionRisk factors = 7 Hs: Heredity (genetic hypocoagulability), History (prior DVT or PE), Hypomobility (fracture, prolonged travel, surgery, obesity), Hypovolemia (dehydration), Hypercoagulability (cancer, smoking), Hormones (pregnancy, oral contraceptive pill [OCP] use), and Hyperhomocysteinemia.

Hint 206

Radiology = CXR may be normal or may show pleural effusion or wedge-shaped infarct; pulmonary angiography is diagnostic, but a higher risk study; spiral CT may detect proximal PE; ventilation-perfusion (V/Q) scan can detect areas of ventilation-perfusion mismatchA positive or negative V/Q scan is diagnostic or rules out PE, but an equivocal scan indicates need for angiographyTreatment = supplemental O2 to maximize saturation; IV fluids or cardiac pressors as needed for hypotension; anticoagulate initially with either low molecular weight heparin (LMWH) or unfractionated heparin (titrated for PTT 1.5–2.5 times normal); patients treated with unfractionated heparin need to be converted to either LMWH or warfarin (given to achieve goal international normalized ratio [INR] 2 -3) for 3–6 months; inferior vena cava filter can be placed if anticoagulation is contraindicated; thrombolysis may be considered for patients with massive PE or those with no cardiac contraindications, recent trauma, or surgery

Front 207

H/P = dyspnea, fatigue, deep chest pain, cough, syncope, cyanosis; digital clubbing, loud S2, JVD, hepatomegalyLabs = increased red blood cell count (RBC) and WBCECG = right ventricular hypertrophyRadiology = CXR shows large pulmonary artery and large right ventricle; echocardiogram useful for measuring pulmonary artery pressure noninvasively and detecting valvular disease; cardiac catheterization is the gold standard test for measuring pressures, but carries greater risks than other studies; PFTs may be useful in diagnosing underlying pulmonary disease

Back 207

Pulmonary hypertensionIncreased pulmonary artery pressure caused by PE, valvular disease, left-to-right shunts, COPD, or idiopathic causesIdiopathic pulmonary hypertension has a high mortality rate within a few years of diagnosis

Hint 207

Treatment = treat underlying condition; supplemental O2 helps maintain blood oxygenation; vasodilators indicated for idiopathic and pulmonary causes to decrease pulmonary vascular resistance; anticoagulants indicated in patients with idiopathic, embolic, or cardiac causes to decrease risk of pulmonary thrombus formation

Front 208

H/P = orthopnea, paroxysmal nocturnal dyspnea, dyspnea; tachycardia, frothy sputum, wheezing, rhonchi, rales, dullness to percussion, peripheral edema, S3 or S4 heart sound, hypertensionLabs = increased brain natriuretic peptide (BNP) or abnormal cardiac enzymes help elucidate a cardiac causeECG = T-wave abnormalities or QT prolongation are common changes and can occur suddenly with acute onset

Back 208

Pulmonary edemaIncreased fluid in lungs caused by increased pulmonary venous pressure and hydrostatic leak of fluid from vesselsCaused by left-sided heart failure, myocardial infarction (MI), valvular disease, arrhythmias, ARDS(pulmonary wedge pressure <18 mm Hg).A pulmonary wedge pressure measured with a Swan-Ganz catheter is suggestive of a cardiac cause for pulmonary edema if >18 mm Hg

Hint 208

Radiology = CXR shows fluid throughout lungs, cephalization of vessels (i.e., increased vascular markings in upper lung fields), Kerley B lines (i.e., prominent horizontal interstitial markings in lower lung fields)Treatment = treat underlying condition; diuretics, salt restriction, O2, morphine, vasodilators; nesiritide improves outcomes in cases with a cardiac cause; pressors may be required to improve cardiac output if perfusion is inadequate; Swan-Ganz catheter placement useful for monitoring response to therapy

Front 209

H/P = possibly asymptomatic; dyspnea, pleuritic chest pain, weakness; decreased breath sounds, dullness to percussion, decreased tactile fremitus, egophonyRadiology = CXR shows blunting of costophrenic angles; decubitus CXR can demonstrate whether fluid is loculated or free flowing; CT is useful for measuring pleural thickness, distinguishing a discrete collection from a diffuse one (e.g., abscess vs. empyema)

Back 209

Pleural effusionSerous or lymphatic fluid collection in pleural space is classified according to protein and lactate dehydrogenase (LDH) content and is caused by changes in hydrostatic and oncotic pressure (transudative), inflammation (exudative), or lymphatic duct rupture (lymphatic)1/4 of pleural effusions are associated with neoplasm

Hint 209

Labs = pleural fluid analysis used for protein and LDH levels (i.e., transudate vs. exudates), glucose (low in TB, malignancy, autoimmune diseases), pH (acidic in malignancy, TB, empyema), amylase (high in pancreatitis, esophageal rupture, some malignancies), triglycerides (high in thoracic duct rupture), complete blood cell count (CBC), Gram stain, and cytologyTreatment = treat underlying condition; relieve pressure on lung with thoracocentesis and chest tube placement; for cases with empyema (i.e., effusion of pus due to infection), a chest tube is required; if recurrent malignant effusion occurs, use pleurodesis (talc or other irritant) to scar the pleural layers together

Front 210

Pleural effusionPleural: Serum Protein Ratio <0.5;Pleural: Serum LDH Ratio <0.6;Total Pleural Protein <3 g/dL

Back 210

Transudateetiology=CHF, cirrhosis, kidney diseases (nephrotic syndrome)

Front 211

Pleural effusionPleural: Serum Protein Ratio >0.5;Pleural: Serum LDH Ratio >0.6;Total Pleural Protein >3 g/dL

Back 211

Exudateetiology=Infection, cancer, vasculitis

Front 212

H/P = unilateral chest pain, dyspnea; decreased chest wall movement, unilateral decreased breath sounds, increased resonance to percussion, decreased tactile fremitus; respiratory distress, decreased Sao2, hypotension, JVD, or tracheal deviation suggest tension pneumothoraxRadiology = CXR shows lung retraction and mediastinal shift away from affected side; tension PTX will demonstrate tracheal deviation

Back 212

Pneumothorax (PTX)Collection of air in pleural space that predisposes patient to pulmonary collapseCan occur spontaneously (less common) or secondary to trauma or a pulmonary medical condition (more common)

Hint 212

TreatmentSmall (<15% lung field) PTX may resolve with supplemental O2 onlyLarger (>15%) PTX requires chest tube placementOpen PTX with small wound is treated with chest tube and occlusive dressingOpen PTX with larger wounds should be treated with attempted closure and should carry a low threshold for intubationTension pneumothorax requires immediate needle decompression (4th or 5th intercostal space at the maxillary line) and chest tube placementRecurrent pneumothorax may require pleurodesis

Front 213

H/P = dyspnea, pleuritic chest pain, weakness; decreased breath sounds, dullness to percussion, decreased tactile fremitus, egophonyLabs = thoracocentesis shows bloody effusion

Back 213

HemothoraxCollection of blood in pleural space caused by trauma, malignancy, TB, or pulmonary infarctionComplications = thrombi formation, fibrosis can occur if blood is not drained from pleural space

Hint 213

Radiology = CXR resembles that for pleural effusion (i.e., lung retraction, mediastinal shift from affected side)Treatment = supplemental O2; chest tube placement; treat underlying cause

Front 214

H/P = nonpleuritic chest pain, dyspnea; dullness to percussion over lung bases, palpable chest wall mass, scoliosis toward lesion

Back 214

Malignant mesotheliomaUncommon tumor occurring on visceral pleura or pericardium with very poor prognosisIncreased incidence with asbestos exposure (occurs 20 years after exposure)

Hint 214

Labs = pleural biopsy is usually diagnostic; thoracocentesis of an associated pleural effusion can be used for cytology studiesRadiology = CXR shows pleural thickening, pleural effusion; chest CT can display extent of local disease; PET scan can be used to detect extrathoracic diseaseTreatment = extrapleural pneumonectomy with adjuvant chemotherapy and radiation therapy; chemotherapy alone used for unresectable disease

Front 215

H/P = fatigue, daytime sleepiness, snoring, gasping or choking during sleep, morning headaches or confusion, impaired daytime function because of sleepiness; obesity common, anatomic abnormalities of palate or pharynx may be visibleLabs = Epworth sleepiness scale is useful for predicting likelihood of sleep apnea as cause for daytime somnolence (score >10 common in sleep apnea); polysomnography is definitive test that measures Apnea Index (AI, average apneic episodes per hour), Sao2, and number of arousals

Back 215

Sleep apneaEpisodic cessation of airflow during sleep leading to desaturations and frequent arousalsTypesObstructive: obstruction of upper airway during sleep with continued respiratory effort; most often associated with obesity or abnormal pharyngeal anatomyCentral: loss of central respiratory drive leads to cessation of airflow and respiratory effortMixed: combines both obstructive and central characteristicsRisk factors = obesity, sedative use; males more than femalesEtiology is unknown, but may be linked to abnormal feedback control during sleep or decreased sensitivity of upper airway muscles to stimulation

Hint 215

TreatmentObstructive = consider weight loss (possibly bariatric surgery) and stop sedative use; continuous positive airway pressure (CPAP) is helpful in chronic cases to maintain airway patency; surgical correction of tonsillar hypertrophy, polyp removal, correction of congenital upper airway deformities, or tracheostomy may be necessary in severe or refractory casesCentral = respiratory stimulants; phrenic nerve pacemaking may be needed in severe casesBariatric surgery is associated with resolution of sleep apnea in 86% of cases.

Front 216

H/P = asymptomatic if mild or slow development; pleuritic chest pain, dyspnea; fever, decreased breath sounds, dullness to percussion over affected areaRadiology = CXR will show fluffy infiltrates in mild cases and lobar collapse in cases of airway obstruction

Back 216

AtelectasisLocalized alveolar collapse; common after surgery (especially abdominal) and anesthesia (generally not clinically serious); can also occur in asthmatics, after foreign body aspiration, or from mass effect (e.g., tumors, pulmonary lesions, or lymphadenopathy)If atelectasis lasts >72 hr, pneumonia is likely to develop.

Hint 216

Treatment = inspiratory spirometry, ambulation, and inpatient physical therapy are important for prevention in the hospital and postoperatively; severe cases require upper airway suctioning or bronchoscopy with deeper suctioning

Front 217

Mechanical VentilationUse=General anesthesia, overdosePatient=No effort

Back 217

Mode=Controlled mechanical ventilation (CMV)

Hint 217

Machine Determines and automatically delivers tidal volume (TV) and rate

Front 218

Mechanical VentilationUse=Weaning patient from ventilatorPatient=Can breathe spontaneously between mechanical breaths

Back 218

Mode=Intermittent mandatory ventilation (IMV)

Hint 218

Machine Determines and automatically delivers TV and rate

Front 219

Mechanical VentilationUse=More comfortable for patient because of attempted synchronization; frequently used in place of IMVPatient=Can breathe spontaneously between mechanical breaths

Back 219

Mode=Synchronized intermittent mandatory ventilation (SIMV)

Hint 219

Machine Machine tries to synchronize rate with patient-initiated breaths; automatically delivers TV and rate

Front 220

Mechanical VentilationUse=Used when patient is more awake and in progressive weaningPatient driven unless no attempts to breathe (backup rate)

Back 220

Mode=Assist-control ventilation (AC)

Hint 220

Machine senses patient's attempt to breathe and delivers full preset TV; backup rate if no spontaneous breaths

Front 221

Mechanical VentilationUse=Used when patient relies less on ventilator; intubation not requiredPatient does all breathing

Back 221

Mode=Continuous positive airway pressure (CPAP)

Hint 221

Machine maintains airway patency to decrease work of breathing

Front 222

H/P = barking cough, inspiratory stridor, dyspnea, nasal congestion; fever, mild pharyngeal erythema, lymphadenopathy; respiratory distress in severe casesRadiology = neck radiographs may show subglottic narrowing of airway (i.e., steeple sign)

Back 222

CroupAcute inflammation of larynx caused by parainfluenzae virus type 1; less commonly, by parainfluenzae virus types 2 and 3, respiratory syncytial virus (RSV) influenza virus, rubeola, adenovirus, or Mycoplasma pneumoniae3 Ss: Seal-bark cough, Subglottic swelling, and Stridor.

Hint 222

Treatment = supportive care (e.g., hydration, humidified air, rest, analgesia); aerosolized epinephrine and inhaled corticosteroids can be used in severe cases to decrease pharyngeal inflammation; with concerns for respiratory distress, the child should be admitted for observationIf child develops stridor at rest, hospitalization and respiratory monitoring is needed.

Front 223

H/P = dysphagia, muffled voice, drooling, soft stridor, anxiety from symptoms; sudden high fever, inspiratory retractions; child may lean forward with hands on knees to aid breathing; erythematous and swollen epiglottisRadiology = neck radiographs show swollen opacified epiglottis that partially obstructs the airway (i.e., thumbprint sign); laryngoscope (only used in controlled situations) can visualize red and swollen epiglottis

Back 223

EpiglottitisRapidly progressive infection of epiglottis and surrounding tissues that can cause airway obstructionMost common in children from 2–7 years of ageCaused by Haemophilus influenzae type B (Hib) infection; can also be caused by streptococcal or other H. influenzae bacteria

Hint 223

Labs = culture from swab of epiglottis can determine causative bacteria (should only be performed if patient intubated)Treatment = keep child calm; admit for close observation and respiratory monitoring; unless airway obstruction is mild, intubate (nasotracheal) to maintain airway patency; antibiotics for 7–10 days; airway obstruction preventing intubation requires emergent tracheostomyIn cases of suspected epiglottitis, examine the patient's throat only in a setting in which prompt intubation is possible because examination of the patient's throat can lead to additional throat irritation and resulting occlusion.

Front 224

H/P = nasal congestion, cough, respiratory distress; wheezing, fever, tachypnea, crackles, prolonged expiration, hyperresonance to percussionRadiology = CXR shows hyperinflation of lungs and patchy infiltrates

Back 224

BronchiolitisViral infection of bronchioles caused by RSV (most cases) or parainfluenzae virus type 3 (less common)Most commonly occurs in winter and spring; usually found in children <2 years of ageComplications = increased risk of developing asthma

Hint 224

Treatment = adequate hydration, humidified air, inhaled corticosteroids and β2-agonists; ribavirin can be used in severe cases to shorten disease course; children with respiratory distress or hypoxemia should be admitted for observation and respiratory monitoring

Front 225

H/P = presentation within 2 days of birth; cyanosis, nasal flaring, expiratory grunting, intercostal retractions, respiratory rate >60 breaths/min, crackles, decreased breath soundsRadiology = CXR shows bilateral atelectasis with ground glass appearance and decreased lung volumes

Back 225

Respiratory distress syndrome of the newbornPreterm infants (e.g., 24–37 wks' gestation and especially before 30 wks' gestation) have surfactant deficiency because of lung immaturity that leads to decreased lung compliance, atelectasis, and respiratory failureComplications = increased risk of developing asthma in childhood compared with other children

Hint 225

Labs = ABG shows increased CO2, decreased O2; amniotic fluid analysis (see Figure 2-9) not usually helpful, but may guide treatment between 34 and 37 wks' gestation by determining fetal lung maturity with the amniotic lecithin:sphingomyelin ratio (always treat for <34 weeks, treatment typically unnecessary for >37 weeks)Treatment = maternal administration of corticosteroids before initiation of labor helps to speed fetal lung maturation; neonatal intensive care unit (ICU) admission appropriate for close observation; supplemental O2 and surfactant replacement therapy mainstays of therapy; intubation should be performed for any neonate not responding to treatment or requiring high levels of O2 to maintain adequate Sao2

Front 226

H/P = meconium stained-amniotic fluid seen during delivery; cyanosis, intercostal retractions; distended chest, tachypnea

Back 226

Meconium aspiration syndromeAspiration of meconium (i.e., fetal stool passed into amniotic sac) predelivery causing obstruction of airways and pneumoniaComplications = pulmonary hypertension can develop if not promptly treated; increased risk of developing asthma during childhood

Hint 226

Labs = consider blood culture to rule out sepsisTreatment = suction nose, mouth, and upper airway at birth; supplemental O2; intubate for worsening respiratory distress; surfactant therapy may be useful for improving respiratory function; consider empiric antibiotic therapy if concerned for development of pneumonia

Front 227

H/P = recurrent pulmonary infections (e.g., Pseudomonas, S. aureus), dyspnea, hemoptysis, chronic sinusitis, cough, meconium ileus at birth, steatorrhea, failure to thrive; cyanosis, digital clubbing, esophageal varices, rectal prolapseLabs = decreased serum Na; sweat test shows increased Na and increased Cl (>60 mEq/L in children, >80 in adults); genetic testing can locate mutation in CF transmembrane conductance regulator (CFTR) gene in suspected cases or in carriers of the gene considering pregnancy

Back 227

Cystic fibrosis (CF)Autosomal recessive disorder caused by defect in chloride-pumping channel in exocrine glands; ducts of exocrine glands (e.g., lungs, pancreas, reproductive glands) become clogged with thick secretionsPresents in childhood and universally fatal, but proper treatment may allow survival into late 20s or early 30sAffects both pulmonary (recurrent infections, chronic sinusitis) and gastrointestinal systems (pancreatic enzyme deficiencies, malabsorption)Risk factors = whites at higher risk than other races

Hint 227

Treatment = deoxyribonuclease (DNase) aids in decreasing the viscosity of secretions; chest physical therapy helps to clear secretions; bronchodilators, non-steroidal anti-inflammatory drugs (NSAID), antibiotics for any suspected pulmonary exacerbation or infection; supplemental pancreatic enzymes and vitamins A, D, E, and K given for malabsorption

Front 228

Tidal volume (TV)

Back 228

Inspiratory volume during Normal respiratioN

Front 229

Inspiratory reserve volume (IRV)

Back 229

Air volume beyond normal tidal volume that is filled during maximal inspiration

Front 230

Inspiratory capacity (IC)

Back 230

Total inspiratory air volumE considering both tidal volume and inspiratory reserve volume (IC = TV + IRV)

Front 231

Expiratory reserve volume (ERV)

Back 231

Air volume beyond tidal volume that can be expired during normal respiration

Front 232

Residual volume (RV)

Back 232

Remaining air volume left in lung ollowing maximal expiration

Front 233

Functional reserve capacity (FRC)

Back 233

Air volume remaining in lungs after expiration of tidal volume (FRC = RV + ERV)

Front 234

Functional vital capacity (FVC)

Back 234

Maximal air volume that can be inspired and expired (FVC = IC + ERV)

Front 235

Total lung capacity (TLC)

Back 235

Total air volume of lungs (TLC = FVC + RV)

Front 236

Risk factors for DVT.

Back 236

stasisendothelial injuryhypercoagulability (Virchow's triad)

Front 237

Criteria for exudative effusion.

Back 237

pleural/serum protein > 0.5pleural/serum LDH > 0.6

Front 238

Causes of exudative effusion.

Back 238

Think of leaky capillaries.MalignancyTBbacterial or viral infectionpulmonary embolism w/ infarctpancreatitis

Front 239

Causes of transudative effusion.

Back 239

Think of intact capillarie.CHFliver or kidney diseaseprotein-losing enteropathy

Front 240

Nornalizing PCO2 in a patient having an asthma exacerbation may indicate?

Back 240

Fatigue & impending respiratory failure

Front 241

dypnealateral hilar lymphadenopathy on CXRnoncaseating granulomasincreased ACEhypercalcemia

Back 241

Sarcoidosis

Front 242

PFT showing decreased FEV1/FVC.

Back 242

Obstructive pulmonary disease (e.g. asthma)

Front 243

PFT showing increased FEV1/FVC.

Back 243

Restrictive pulmonary disease

Front 244

Honeycomb patten on CXR. Diagnosis?Treatment?

Back 244

Diffuse interstitial pulmonary fibrosis.Supportive care.Steroids may help.

Front 245

Treatment for SVC syndrome.

Back 245

Radiation

Front 246

Treatment for mild, persistent asthma.

Back 246

Inhaled beta-agonists & inhaled corticosteroids

Front 247

Acid-base disorder in pulmonary embolism.

Back 247

Hypoxia & hypocarbia

Front 248

Non-small cell lung cancer (NSCLC) associated with hypercalcemia.

Back 248

Squamous cell carcinoma

Front 249

Lung cancer associated w/ SIADH.

Back 249

Small cell lung cancer (SCLC)

Front 250

Lung cancer highly related to cigarette

Back 250

Small cell lung cancer (SCLC)

Front 251

A tall white male presents w/ acute shortness of breath. Diagnosis?Treatment?

Back 251

Spontaneous pneumothorax.Spontaneous regression.Supplemental O2 may be helpful.

Front 252

Treatment of tension pneumothorax.

Back 252

Immediate needle thoracostomy

Front 253

Characteristics favoring carcinoma in an isolated pulmonary nodule.

Back 253

Age > 45-50 yrslesions new or larger in comparison to old filmsabsence of calcifcation or irregular calcificationsize > 2 cmirregular margins

Front 254

Hypoxemia & pulmonary edema w/ normal pulmonary capillary wedge pressure.

Back 254

ARDS

Front 255

Increased risk of what infection w/ silicosis?

Back 255

Mycobacterium tuberculosis

Front 256

Causes of hypoxemia.

Back 256

right-to-left shunt hypoventilation low inspired O2 tension diffusion defect V/Q mismatch

Front 257

Classic CXR findings for pulmonary edema

Back 257

cardiomegaly prominent pulmonary vesselsKerley B lines"bat's wing" appearance of hilar shadowsperivascular & peribronchial cuffing

Front 258

_x0001_ SymptomsUnilateral, throbbing, visual and autonomic disturbances, nausea.Basilar migraine may present with ataxia, vertigo, dysarthria._x0001_ DiagnosisTypical symptoms in young adult, positive family history often, 75%of cases are women. Increased incidence of motion sickness and in-fantile colic.

Back 258

Migraine_x0001_ Description• Classic migraine—unilateral throbbing headache with aura.• Common migraine—subtle onset, no aura, represents 80% of cases_x0001_ PathophysiologySerotonergic neurons in brain stem raphe involved. Vasomotorchanges. Spreading depression of Leao (neuronal depression). Cor-tical oligemia, extracranial vasodilation.

Hint 258

_x0001_ Treatment Steps1. Pharmacotherapy—acute headache: ergot alkaloids, serotonin(5-HT) agonists, prochlorperazine, metoclopramide.2. Preventive treatment: β-blockers, sodium valproate, topiramate,gabapentin, lamotrigine, methysergide (potential for retroperi-toneal fibrosis with long-term use), calcium channel blockers, an-tidepressants, nonsteroidal anti-inflammatory drugs (NSAIDs),cyproheptadine.3. Avoid alcohol, tyramine (cheese), chocolate, citrus, onions, andnitrite.

Front 259

_x0001_ SymptomsSevere pain in short episodes without aura, for weeks to months,then remits, ipsilateral lacrimation, nasal congestion, conjunctivalinjection, nasal congestion, dilated superficial temporal artery._x0001_ DiagnosisTypical symptoms, men more often (95%), worse with alcohol andsleep.

Back 259

Cluster Headache_x0001_ DescriptionVascular headache, also known as histamine cephalalgia, Horton’sheadache, migrainous neuralgia.

Hint 259

_x0001_ Treatment Steps1. Pharmacotherapy—acute headache: ergot alkaloids, serotonin(5-HT) agonists, prochlorperazine, metoclopramide.2. Preventive treatment: β-blockers, sodium valproate, topiramate,gabapentin, lamotrigine, methysergide (potential for retroperi-toneal fibrosis with long-term use), calcium channel blockers, an-tidepressants, nonsteroidal anti-inflammatory drugs (NSAIDs),cyproheptadine.3. Avoid alcohol, tyramine (cheese), chocolate, citrus, onions, andnitrite.2. Also prednisone, oxygen, lithium.

Front 260

_x0001_ SymptomsTemporal headache, focal tenderness superficial temporal/occipitalarteries, vision loss, malaise. Can be associated with polymyalgiarheumatica._x0001_ DiagnosisClinical suspicion, elevated erythrocyte sedimentation rate (ESR),biopsy of temporal artery.patientover age 50 (but oftenmuch older) whopresents with unilateralheadache in temporalregion, or eye pain

Back 260

Temporal Arteritis (Giant Cell)_x0001_ DescriptionInflammatory systemic illness in elderly. Medical emergency._x0001_ PathologyMononuclear cell and giant-cell infiltrates in cranial arteries. Skip le-sions.

Hint 260

_x0001_ Treatment StepsCorticosteroids Treatment with steroidsmust be startedimmediately to preventloss of vision.• Surgical biopsy isdefinitive for diagnosis,and although startingsteroids empirically mayalter biopsy results, it isoften done to preventblindness.

Front 261

_x0001_ SymptomsThose of increased intracranial pressure without tumor, headache,visual disturbances, nausea, vomiting, dizziness._x0001_ DiagnosisClinical seting (headache, papilledema, no focal neurologic find-ings, obese female). Magnetic resonance imaging (MRI) more sensi-tive to look for hydrocephalus, rule out tumor or dural sinus veinthrombosis. Lumbar puncture shows elevated opening pressure.

Back 261

Benign Intracranial Hypertension(Pseudotumor Cerebri)_x0001_ PathologyDecreased cerebrospinal fluid outflow conductance.

Hint 261

_x0001_ Treatment Steps1. Acetazolamide, diuretics.2. Prednisone.3. Serial lumbar punctures.4. Optic nerve sheath incision, lumboperitoneal shunts.

Front 262

_x0001_ SymptomsBrief episodes of pain in fifth cranial nerve distribution, third andsecond divisions_x0001_ DiagnosisOnset after 40, more often in women, may coexist with multiple scle-rosis (MS); history is diagnostic, may have facial trigger points butno sensory impairment.

Back 262

Trigeminal Neuralgia (Tic Douloureux)_x0001_ PathologyDegenerative changes gasserian ganglion. Compression of trigemi-nal nerve by vascular loops causing demyelination. MS; demyelina-tion of root entry zone.

Hint 262

_x0001_ Treatment Steps1. Phenytoin, carbamazepine, baclofen, gabapentin, amitriptyline,lamotrigine.2. Alcohol nerve block.3. Microvascular decompression.4. Percutaneous radiofrequency nerve thermocoagulation.

Front 263

Impending loss of consciousness secondary to inadequate cerebralperfusion.

Back 263

Syncope and PresyncopeEtiology vascular or cardiac, not neurologic. May be due to hyperventilation, orthostatic hypotension, vasovagal, micturition

Front 264

Disorder of balance system, dizziness when standing and walking,

Back 264

Dysequilibriummultiple possible central nervous system (CNS) causes. Chronic andcommon in elderly.

Front 265

Sensation of movement, due to abnormality of the peripheral orcentral vestibular system pathways. Nystagmus may be present. Pe-ripheral nystagmus is unidirectional and suppressed by fixation.Central nystagmus may be multidirectional and is never suppressedby fixation.

Back 265

Vertigodisorders resulting in vertigoinclude vestibular neuronitis, labyrinthitis, posttraumatic brain stemtransient ischemic attack (TIA), MS, posterior fossa tumor, and basi-lar artery migraine

Front 266

hearing loss, tinnitus, and vertigo.

Back 266

Ménière’s disease

Front 267

vertigo aggravated by change in head position, sneezing, noises

Back 267

Perilymph fistulaoval window tear resulting

Front 268

premonitory phase followed by immediate lossof consciousness, tonic, clonic, and postictal (confusion) phases.Electroencephalogram (EEG) hallmark is immediate bihemisphericdischarges

Back 268

Tonic and/or clonicGeneralized Epileptic Seizures

Front 269

brief loss of consciousness (5–10 seconds), sud-den blank stare, abrupt cessation of activity; clonic movements, au-tomatisms such as lip smacking. EEG three per second spike-and-wave pattern.

Back 269

Absence seizuresGeneralized Epileptic Seizures

Hint 269

Drug of choice: ethosuximide.

Front 270

sudden generalized or focal muscle jerk, EEG dischargeconcurrent with jerk

Back 270

MyoclonicGeneralized Epileptic Seizures

Front 271

1 to 2 sec. Drop attacks limited or generalized, .

Back 271

Atonic seizuresGeneralized Epileptic Seizuressecondary to diffuse brain disease

Front 272

infantile spasms (sudden extensor/flexor trunk movements) psychomotor retardation and EEG hyparrhythmia (disorganized high-voltage slow waves, spikes, and sharp waves)

Back 272

West syndromeGeneralized Epileptic Seizurespre- & postnatal causes including genetic disorders, injuries, infections,metabolic disorders.

Hint 272

Adrenocorticotropic hormone (ACTH), valproic acid or clonazepam

Front 273

less abrupt onset, longer, loss of postural tone, as-sociated with other seizure types; EEG background abnormal, ictal0.5- to 2.5-Hz spike-and-wave discharges.

Back 273

Atypical absenceGeneralized Epileptic Seizures

Front 274

no impairment of consciousness.start in one motor cortical area—may spread with progressive jerking (jacksonian seizures)

Back 274

Simple partial sezures, Motor

Front 275

no impairment of consciousness.tingling, numbness, sensation of movement or absenceof body part.

Back 275

Simple partial sezures, Sensory, Parietal

Front 276

no impairment of consciousness.flashes of light, hemianopsia, scotomata. Visual associa-tion cortex, complex images—micropsia, macropsia, distortions.

Back 276

Simple partial sezures, Sensory, Occipital

Front 277

no impairment of consciousness.auditory, olfactory hallucinations, emotional or psy-chic phenomena, memory or cognitive distortions (déjà vu),time distortions, detachment, affective (fear, depression)

Back 277

Simple partial sezures, Sensory, Temporal

Front 278

impaired level of awareness and con-sciousness, amnesia for event, automatisms may occur.

Back 278

Complex partial seizuresFocal Epilepsy

Front 279

a. Benign childhood epilepsy with centrotemporal spikes; stops inadolescence—somatosensory, tonic/tonic–clonic activity involv-ing face to arm, generalized with nocturnal seizures.b. Childhood epilepsy with occipital paroxysms (spikes)—visualseizures while awake, motor seizures during sleep.

Back 279

Partial epileptic syndromesFocal Epilepsy

Front 280

weakness in a part of the body after a seizure

Back 280

Todd’s postictal paralysisreflects a partial seizurehaving taken place

Front 281

Continued or recurrent seizures of any type with unconsciousnessfor 20 or more minutes

Back 281

Status Epilepticus

Hint 281

Treat as medical emergency, intravenous(IV) lorazepam (binds γ-aminobutyric acid [GABA]A receptor) followed by IV phenytoin

Front 282

quadriplegia and lower cranial nerve paralysis, but conscious with higher mental activity intact.

Back 282

Locked-in syndrome

Front 283

Patient cannot be aroused, total unresponsivenesmay demonstrate response to noxious stimuli

Back 283

COMA_x0001_ PathologyDiffuse cerebral hemisphere dysfunction and/or involvement of thebrain stem ascending reticular activating system.• Trauma. History of injury. Epidural hematoma: lucid interval. Sub-dural: depressed consciousness, then focal findings.• Vascular disease. Sudden onset, nuchal rigidity, bloody cerebrospinal fluid (CSF).• Neoplasm. Focal signs, papilledema.• Infection. Cerebrospinal fluid increased protein normal or low CSFglucose.• Metabolic. Abnormal labs.

Hint 283

_x0001_ Treatment Steps1. Establish airway, and IV line.2. Determine cardiovascular status, history, and physical.3. Obtain full lab, skull x-ray, computed tomography (CT), and/orMRI.4. May need lumbar puncture.5. Give thiamine, dextrose, and possibly naloxone.6. If cerebral edema or increased intracranial pressure, restrict fluids,hyperventilate, mannitol, and steroids.

Front 284

patient in coma, but appears awake

Back 284

Akinetic mutism (coma vigile)

Front 285

coma (lesion localization)hyperpnea alternating with apnea

Back 285

Cheyne–Stokes respirationbilateral cerebral hemisphere damage

Front 286

coma (lesion localization)long inspiration then pauseorataxic (chaotic) breathing

Back 286

Apneustic respiration or ataxic (chaotic) breathinglower pontine lesions

Front 287

coma (lesion localization)extension/adduction of armsand legs

Back 287

Decerebrate posture. Midbrain lesion

Front 288

coma (lesion localization)flexion arms, wrists, and fingers

Back 288

Decorticate posture. Lower diencephalon lesion

Front 289

sudden onset of a focal neurologic deficit due to cerebrovas-cular disease, lasting more than 24 hours.

Back 289

StrokeTo identify cause of stroke, the following tests are usually completed:• Carotid ultrasound.• Echocardiogram (transesophageal echocardiogram done incertain settings).• Fasting lipid panel.• Hypercoagulability workup may be indicated in certaincases, particularly young individuals with no other source of stroke

Front 290

focal, abrupt in onset, usually lasts less than 1 hour; resolvewithin 24 hours

Back 290

TIAGreatest risk for stroke in days to weeks.

Front 291

stroke or TIA (origin)abrupt onset while activePatients rarely lose consciousness

Back 291

Cerebral Embolismmost commonsource of embolism is the heart; less common peripheral arterialembolization.

Front 292

stroke or TIA (origin)abrupt onset while activemay lose consciousness

Back 292

Subarachnoid Hemorrhageaneurysm at circle of Willi

Front 293

stroke or TIA (origin)abrupt onset while activemay lose consciousness; CT positive for hematoma

Back 293

Intraparenchymatous Hemorrhage

Front 294

stroke or TIA (origin)10% preceded by TIA, often during sleep; rarely loseconsciousness.May have normal CT and lumbar puncture early;rarely have headache

Back 294

Thrombotic

Front 295

Ischemic Stroke (artery?)contralateral hemiplegia/paresis. Domi-nant hemisphere—nonfluent or Broca’s aphasia from upper-divisionocclusion.Wernicke’s (fluent) aphasia from lower-division lesions.

Back 295

Middle cerebral artery

Front 296

Ischemic Stroke (artery?)contralateral leg paralysis, abulia, aki-netic mutism, sphincter incontinence

Back 296

Anterior cerebral artery

Front 297

Ischemic Stroke (artery?)contralateral weakness or sensory loss, speechdisturbance, ipsilateral visual loss

Back 297

Carotid artery

Front 298

Ischemic Stroke (artery?)contralateral homonymous hemianopia, cortical blindness, prosopagnosia, alexia without agraphia.

Back 298

Posterior cerebral

Front 299

Ischemic Stroke (artery?)ataxia, hemiplegia, horizontal gaze, palsy, nystagmus vertigo, deafness, dizziness

Back 299

Vertebrobasilar

Front 300

Ischemic Stroke (artery?)ataxia, dizziness, nausea, vomiting

Back 300

Cerebellar

Front 301

Ischemic Stroke (artery?)pure motor or sensory strokes, clumsy hand syndrome may be seen

Back 301

Lacunar infarct—due to lipohyalinosis

Front 302

Ischemic Stroke

Back 302

_x0001_ Risk Factors• Nonmodifiable—race, age, gender, family history prior TIA orcerebrovascular accident (CVA).• Modifiable—hypertension, diabetes mellitus, smoking, alcoholabuse, oral contraceptives, cardiac disease, prior stroke, lipoproteinabnormalities, elevated homocysteine and C-reactive protein, coag-ulopathies.

Hint 302

_x0001_ Treatment Steps1. Prevention—treat modifiable risk factors (above).2. TIA—antiplatelet aggregating drugs (aspirin, ticlopidine, clopi-dogrel).3. Acute ischemic infarction—protect airway, prevent aspiration,avoid aggressive blood pressure (BP) control. Treat BP slowly ifover 170/100 mm Hg. Treat hyperglycemia, reduce fever. Throm-bolysis in infarcts less than 3 hours old with tissue plasminogenactivator. Cerebral edema peaks in 2 to 7 days; treat with modestfluid restriction, intubation and hyperventilation, mannitol.4. Elective carotid endarterectomy if carotid stenosis present.

Front 303

headache, vomiting, decreasedlevel of consciousnessStroke (cause)

Back 303

Hypertensive intracerebral hemorrhage

Front 304

Hypertensive intracerebral hemorrhage (location?)Unusual eye signs

Back 304

thalamic hemorrhage

Front 305

Hypertensive intracerebral hemorrhage (location?) pin-point reactive pupils, coma, quadriplegia, ophthalmoplegia, decerebrate posturing

Back 305

Pontine hemorrhage

Front 306

Hypertensive intracerebral hemorrhage (location?)vertigo,headache, vomiting, and ataxia.

Back 306

Cerebellar bleed

Front 307

Hypertensive intracerebral hemorrhage (location?)hydrocephalus

Back 307

Ventricular extension associated with poor prognosis.

Front 308

Sudden severe headache, meningeal irrita-tion; exam may be normal

Back 308

Subarachnoid hemorrhage—caused by saccular aneurysm or vascular malformation

Front 309

Hemorrhagic Stroke (work up/treatment?)Other causes of bleeding include arteriovenous malformation, tu-mor, anticoagulant therapy, cocaine abuse, cerebral amyloid an-giopathy, angiitis

Back 309

Initial test of choice—CT scan. Do lumbar puncture only if CT not available, and check for papilledema before doing lumbar puncture.

Hint 309

_x0001_ Treatment Steps1. Control BP.2. Treat seizures.3. Control raised intracranial pressure (ICP).4. Surgery in selected cases—ventriculostomy to decrease ICP andremove blood, hemorrhage removal in some instances (cerebellum, putamen, lobar).

Front 310

_x0001_ SymptomsOptic neuritis, vertigo, paresthesias, sensory loss, pain, incoordination,bladder dysfunction, nystagmus, weakness in 50%, trigeminal neural-gia, diplopia, internuclear ophthalmoplegia, characteristically bilateral.

Back 310

Multiple Sclerosis_x0001_ DescriptionMultiple areas of neurologic deficits, peak age 20 to 24. Increased in-cidence in women and north temperate latitudes, etiology unknown,possibly autoimmune. Fewer exacerbations during pregnancyDIAGNOSIS OF MS• Signs and symptomstypical of the disease areneeded and must bepresent at two differentpoints in time.• Testing will help confirmthe diagnosis.• Demyelinating plaquesseen on MRI ofbrain/spinal cord.• CSF often revealsoligoclonal bands.• Increased latency invisual evoked response(VER), brain stemauditory evokedresponse (BAER), orsomatosensory evokedpotential (SSEP)

Hint 310

_x0001_ Treatment Steps1. Acute exacerbations: Intravenous or oral steroids.2. Prophylaxis: Interferon-β (Avonex, Betaseron, Rebif), interferon-α (Intron A), or glatiramer acetate (Copaxone).3. Symptomatic treatment: Spasticity—Lioresal, Tizanidine, Dantrium;bladder—oxybutinin, hyoscyamine, antiseptics (vitamin C, meth-enamine); pain—carbamazepine, gabapentin, amitriptyline, lam-otrigine.

Front 311

Papillitis, swelling of the optic nerve head may occur. May cause acute visual lossDecreased visual acuity and color vision, scotomata, ocular pain. Ab-normal VER, visual fields, and contrast sensitivity.

Back 311

Optic Neuritis_x0001_ DescriptionInflammation of the optic nerve, often from optic nerve demyelination. Episode of optic neuritis may precede MS. _x0001_ DiagnosisMRI may demonstrate T2-weighted and gadolinium-enhancing lesions of optic nerve.Brain or spinal cord MRI abnormalities—greater risk of MS with twoor more

Hint 311

_x0001_ Treatment StepsIntravenous methylprednisolone (Solu-Medrol). Interferon-β prohylaxis with 2 or more MRI lesions.

Front 312

_x0001_ SymptomsHeadache, stiff neck, confusion, seizures, fever, coma. Focal andmultifocal signs. Mortality 10–30%.postinfectious and postvaccinal

Back 312

Acute Disseminated Encephalomyelitis_x0001_ DescriptionMonophasic, mostly postinfectious and postvaccinal

Hint 312

_x0001_ Treatment StepsCorticosteroids.

Front 313

_x0001_ SymptomsProgressive ascending weakness, areflexiaFrequently preceded by upper respiratory or gastroin-testinal (GI) infection (Campylobacter jejuni), surgery, immunization.Linked to Epstein–Barr virus (EBV), cytomegalovirus (CMV), human immunodeficiency virus (HIV)._x0001_ DiagnosisHigh CSF protein, with few cells, short duration of progression;nerve conduction studies. With HIV infection, CSF pleocytosis isfound.

Back 313

Guillain–Barré Syndrome—A PeripheralNeuropathy_x0001_ DescriptionAcute inflammatory polyradiculoneuropathy in young to middle-aged adults. _x0001_ PathologyEndoneurial perivascular mononuclear cell infiltration; multifocal root and nerve demyelination

Hint 313

_x0001_ Treatment StepsSpontaneous recovery may occur, plasmapheresis, or intravenous im-munoglobulin.

Front 314

_x0001_ SymptomsHeadache, fever, stiff neck. Minimal neurologic signs in viral menin-gitis, which is a benign self-limited disorder and also termed asepticmeningitis. Positive Kernig’s and Brudzinski’s signs.

Back 314

Acute Meningitis_x0001_ DiagnosisGram stain and culture of CSF. CSF protein over 50, viral; in bacte-rial or fungal up to 400. Hypoglycorrhachia (CSF glucose less than40% of serum level) suggests bacterial cause. Tuberculous (charac-teristically lymphocytic meningitis) active pulmonary disease in onethird, positive purified protein derivative (PPD) in 50%_x0001_ Pathology1. Neonatal—group B streptococcus, Escherichia coli.2. Early childhood—Haemophilus influenzae, Streptococcus pneumoniae,and Neisseria meningitidis.3. Young adults—Neisseria meningitidis (petechial or ecchymotic rashoften), S. pneumoniae, H. influenzae.4. Nosocomial—Gram-negative bacteria and Staphylococcus aureus.5. Immunosuppressed—Listeria monocytogenes, S. pneumoniae, H. in-fluenzae, Nocardia, Mycobacterium tuberculosis, Cryptococcus neofor-mans.6. HIV patients—acute aseptic meningitis.7. Viral meningitis—most common agent is mumps; enterovirus ismost common viral group.

Hint 314

_x0001_ Treatment Steps1. Toxoplasma—pyrimethamine plus sulfadiazine.2. Brucella—tetracycline and aminoglycoside. Chronic neurobrucel-losis––rifampin, trimethoprim–sulfamethoxazole, doxycycline.3. Neonatal—ampicillin and gentamicin.4. Adults—ceftriaxone or ampicillin.5. Tuberculous—isoniazid, ethambutol, rifampin, pyrazinamide.6. Fungal—amphotericin B.• Newer studies havesuggesteddexamethasone may beuseful in acute bacterialmeningitis if given beforeor with first dose ofantibiotics.• Prophylaxis (rifampin orciprofloxacin) is given toclose contacts ofpatients with meningitisdue to N. meningitidis,rifampin, or ciprofloxacin

Front 315

_x0001_ SymptomsTabes dorsalis, general paresis, gumma, optic atrophy, cerebrovascu-lar disease from invasion of leptomeninges with Treponema pallidum.Neurosyphilis most often is asymptomatic.

Back 315

Neurosyphilis

Hint 315

_x0001_ Treatment StepsHigh-dose parenteral penicillin

Front 316

hypotension, fever, headache, chills, and tachycardia in first 24 hours of treatment of neurosyphilis

Back 316

Jarisch–Herxheimer reactionrelease of treponemal products; not a penicillinreaction

Front 317

Infection spread from paranasal sinuses and middle earmarked peripheral leukocytosis.

Back 317

Empyema (Subdural)treptococcusmost often

Front 318

_x0001_ SymptomsFocal signs and acute febrile illness, seizures and coma, or depressed state of consciousness. Headache, fever, and nuchal rigidity._x0001_ DiagnosisAseptic CSF, lymphocytic CSF with normal glucose

Back 318

Viral Encephalitis_x0001_ DescriptionMortality of 10%_x0001_ PathologyCaused by mumps, herpes simplex type 1, lymphocytic choriomenin-gitis, arboviruses, EBV. Mouse and hamster exposure linked to lymphocytic choriomeningitis

Hint 318

_x0001_ Treatment StepsTreat edema and seizures

Front 319

respiratory spasms, dysphagia–hydrophobia

Back 319

Rabies—brain stem encephalitis, incubation 30 to 60 days or more fatal in acute stage in95%

Front 320

an acute febrile illness w/ evidence of lower motorneuron paralysis

Back 320

Polio—etiology: enteroviruses that damage anterior horn cells of spinal cord

Front 321

most common opportunisticCNS pathogen in acquired immune deficiency syndrome (AIDS)

Back 321

Toxoplasmosis—intracellular parasite

Front 322

Ataxia and myoclonus, dementia

Back 322

Creutzfeldt–Jakob, kuru

Front 323

Elevated gamma globulin and measles antibodies in CSF

Back 323

Subacute sclerosing panencephalitis

Front 324

Due to SV40-PML

Back 324

Progressive multifocal leukoencephalopathy (PML)

Front 325

temporal lobe localizationCNS infection

Back 325

Herpes simplex encephalitis

Hint 325

treat with acyclovir

Front 326

progressive muscle weaknessand atrophydiagnosis by family history, weakness, muscle biopsy,probable death by age 20. Elevated creatine kinase (CK).

Back 326

Duchennedue to mutation on X chromosome (dystrophin gene;Xp21 locus)

Front 327

NEUROMUSCULAR DISEASEautosomal recessive and dominant forms

Back 327

Limb–girdle

Front 328

thinning face muscles, electromyogram (EMG) shows adecremental pattern, and irregular after potentials. Autosomal domi-nant (chromosome 19q. Expanded CTG repeats in myotonin pro-tein kinase

Back 328

Myotonic

Hint 328

Treat with phenytoin sodium (Dilantin).

Front 329

NEUROMUSCULAR DISEASEFascioscapulohumeral

Back 329

autosomal dominant. No carriers

Front 330

_x0001_ SymptomsWeak with activity, fatigue, ocular symptoms; facial muscles, voice,limb muscles, and respiration can be affected._x0001_ DiagnosisTensilon test, electromyogram—repetitive nerve stimulation, posi-tive antibodies to acetylcholine receptor.

Back 330

Myasthenia Gravis_x0001_ DescriptionAutoantibodies against acetylcholine receptor. Associated withthymic hyperplasia and thymoma. Women more than men

Hint 330

_x0001_ Treatment Steps1. Cholinesterase inhibitors.2. Steroids.3. Plasmapheresis.4. Thymectomy.Thymectomy may offer acure to patients withmyasthenia gravis (MG).Thymectomy is offered toall patients with a thymomaand patients aged 10–55without a thymoma butwith generalized MG5. Immunosuppressants, IV immunoglobulin

Front 331

_x0001_ SymptomsLimb weakness without cranial muscle weakness and absence ofdeep tendon reflexes. Found with small cell lung cancer or as autoimmune disease._x0001_ DiagnosisResponse to repetitive stimulation (increasing action potential)

Back 331

Eaton–Lambert Syndrome_x0001_ DescriptionFacilitating neuromuscular transmission disorder due to autoanti-bodies against presynaptic neuromuscular voltage-gated calciumchannels

Hint 331

_x0001_ Treatment Steps Guanidine. Calcium channel antagonists are contraindicated.

Front 332

_x0001_ SymptomsBegin 12–36 hours after ingestion of exotoxin in contaminatedfood. Blurred vision, dilated fixed pupil, flaccid quadriplegia, dysphagia, dysarthria, respiratory paralysis, dry mouth.

Back 332

Botulism_x0001_ DescriptionToxin of Clostridium botulinum blocks acetylcholine release._x0001_ DiagnosisIsolate toxin from stool, stomach, or food. Spores also found inhoney. EMG—decreased compound muscle action potentials; post-tetanic facilitation

Hint 332

_x0001_ Treatment Steps1. Cathartics.2. Trivalent antitoxin (A, B, E).3. Quinidine.4. Supportive therapy.

Front 333

predominantly distal weakness, cardiacconduction problems, cataracts, testicular atrophy, endocrine dys-function, increased sensitivity to medications which depress respiratory drive, ptosis, temporalis and masseter muscle wasting.

Back 333

Myotonic dystrophy

Front 334

Impaired muscle relaxation

Back 334

Myotonia congenita

Hint 334

treat with phenytoin

Front 335

eosinophilia, weakness, myalgiaundercooked pork mostcommon source

Back 335

Trichinosis_x0001_ DescriptionNematode Trichinella spiralis infection,

Hint 335

_x0001_ Treatment StepsThiabendazole, mebendazole.

Front 336

_x0001_ Symptoms/DiagnosiMuscle spasms, trismus (lockjaw), facial muscle spasm (risus sardon-icus), opisthotonos, autonomic dysfunction. Clinical diagnosis

Back 336

etanus_x0001_ DescriptionLockjaw, intense motor neuron activity._x0001_ PathologyCaused by neurotoxin (tetanospasmin) from Clostridium tetani, agram-positive coccus, which inhibits spinal inhibitory interneurons.

Hint 336

_x0001_ Treatment Steps1. Cleaning and debridement of infected site.2. Antibiotics.3. Antitoxin (human hyperimmune globulin).4. Skeletal muscle relaxants (diazepam).

Front 337

_x0001_ SymptomsIdiopathic, acute, peripheral facial weakness; may have ipsilateralhyperacusis and decreased taste._x0001_ DiagnosisInexcitable facial nerve, denervation of facial muscles after 2–3weeks.

Back 337

Bell’s Palsy

Hint 337

_x0001_ Treatment StepsSupportive treatment Artificial tears to prevent corneal drying. Of-ten self-limited. If patients present early, steroids and/or antiviral medications may be helpful.

Front 338

middle-age rapid progressionof weakness. Combination of upper (spasticity, hyperreflexia, emo-tional lability) and lower (atrophy, weakness, cramps, fasciculations)neuron involvement. Bulbar and respiratory weakness in 50%

Back 338

Amyotrophic lateral sclerosis (ALS)Familial ALS has mutation forsuperoxide dysmutase gene

Hint 338

Treated with riluzole

Front 339

floppy infant, delayed milestones, progressive atrophy, respiratoryand swallowing problems

Back 339

Type 1 proximal spinal muscular atrophy (Werdnig–Hoffmann)Autosomal recessive, deletions in neu-ronal apoptosis inhibitory gene in two-thirds.

Front 340

Weakness,onset age 20–40, muscle cramps, gynecomastia, dysphagia, dysarthria

Back 340

Bulbospinal muscular atrophy (Kennedy’s disease)X-linked recessive, increased CAG repeats in androgen receptor gene

Front 341

_x0001_ SymptomsProgressive emotional or intellectual decline associated with chorea,abnormalities in gait, ocular motor function, and dexterity. Onset in fourth or fifth decades in most. Patients live an average of 15 years after diagnosis.

Back 341

Huntington’s Disease_x0001_ DescriptionChorea, personality change, psychiatric syndromes, progressive de-mentia. Autosomal dominant with expanded CAG repeat sequence in huntingtin gene._x0001_ DiagnosisExam, family history._x0001_ PathologyCaudate nucleus and cerebral cortex atrophy, neuronal loss andgliosis, and decreased GABA and acetylcholine have been noted along with spared somatostatin–neuropeptide Y neurons.

Hint 341

_x0001_ Treatment StepsNo cure but dopaminergic antagonists: presynaptic—tetrabenazine,reserpine; postsynaptic—haloperidol (Haldol).

Front 342

_x0001_ SymptomsNeurologic—tremor, incoordination, ataxia, akinesia, dysarthria,dysphagia, dystonia.Hepatic—hepatitis, which may be acute or chronic; cirrhosis.Ocular—Kayser–Fleischer ring in Descemet’s membrane of corneanoted (rusty brown ring at limbus).Psychiatric—variable presentation._x0001_ DiagnosisHigh serum copper and high urine copper. Slit lamp exam, lowserum ceruloplasmin, and elevated 24-hour urine copper; liverbiopsy and copper quantitation are also helpful. Abnormal liverfunction tests. Aminoaciduria. MRI—cerebral atrophy, putaminal,thalamic, and brain stem hypodensities. Pathology––excess copperdeposits in liver and brain.

Back 342

Wilson’s Disease (Hepatolenticular Degeneration)_x0001_ DescriptionChromosome 13 autosomal recessive disorder of copper metabolism(mutations in copper-transporting P-type ATPase), characterized bydeficient ceruloplasmin, elevated urinary copper excretion. Presentsin adolescence or early adulthood

Hint 342

_x0001_ Treatment StepsD-penicillamine. Adverse effects of therapy include hypersensitivity,fever, nephrotic syndrome, myasthenia gravis, Goodpasture syn-drome, bone marrow suppression (agranulocytosis and thrombocy-topenia), and collagen vascular disorders.

Front 343

_x0001_ SymptomsCharacterized by resting tremor (pill-rolling—5–7 Hz), cogwheelrigidity, bradykinesia, impaired postural reflexes, masked facies, flexed posture, hypophonia._x0001_ DiagnosisClinical exam. Reduced 6-[18F]-fluorolevodopa in striata withpositron-emission tomography (PET)

Back 343

Parkinson’s Disease_x0001_ DescriptionAn idiopathic extrapyramidal movement disorder affecting the el-derly. Reduced activity complex I mitochondrial electron transportchain. Mutation in α-synuclein gene in familial Parkinson’s disease_x0001_ PathologyDepigmentation, neuronal loss and gliosis in substantia nigra andpigmented nuclei. Cytoplasmic inclusion (Lewy) bodies. Results inreduced striatal dopamine. Associated decreased activity complex I mitochondrial electron transport chain.

Hint 343

_x0001_ Treatment Steps1. Levodopa/carbidopa (Sinemet), toxicity with levodopa: dyskine-sias, hallucinations, confusion.2. Anticholinergics, amantadine.3. Dopamine agonists (bromocriptine, pergolide, pramipexole,ropinirole) particularly late.4. Catechol-O-methyltransferase (COMT) inhibitors prolong L-dopa availability.5. Pallidotomy and deep brain stimulation for end-stage disease

Front 344

methylphenyltetrahydropyridine (MPTP); neuroleptics block striatal dopamine receptor sitesIatrogenic Dyskinesias

Back 344

Drug-induced parkinsonism

Front 345

linguofasciobuccal, choreiformIatrogenic Dyskinesias

Back 345

Tardive dyskinesia

Front 346

levodopaIatrogenic Dyskinesias

Back 346

Dopamine agonist-induced chorea

Front 347

inappropriate cocontraction of antagonistic muscles, re-sulting in repetitive twisting movements.

Back 347

Dystonia

Hint 347

Focal dystonias treated withbotulinum toxin injection: generalized with trihexiphenidyl (Ar-tane)

Front 348

random twitching or jerking, excessive, involuntary, pur-poseless movements

Back 348

Chorea

Front 349

oromandibular dystonia

Back 349

Blepharospasm(Meige syndrome)

Front 350

most frequent focal dystonia, involving neckmuscles. Intermittent or sustained head deviation

Back 350

Spasmodic torticollis

Front 351

distal upper extremity, postural or action tremor; is of-ten progressive. May be familial (autosomal dominant with variablepenetrance)

Back 351

Tremor (Essential)

Hint 351

Treatment includes propranolol, primidone, topira-mate. Alcohol responsive

Front 352

Rapid jerking movement

Back 352

Myoclonus

Hint 352

treat primary cause when known. Clonazepam, 5-hydroxytryptophan (5-HTP) and valproic acid often used

Front 353

Sudden loss of postural toneClassically described as a “flap.” Patient has arms outstretched, palms out, but cannot keep hands still.

Back 353

AsterixisOccurs in metabolic encephalopathies(uremic, hepatic), drug intoxications, and structural brain lesions.

Front 354

_x0001_ SymptomsMemory loss, language and visuospatial impairments, mood distur-bance, delusions, hallucinations, changes in personality and behav-ior. Generalized seizures (10–20%).

Back 354

Alzheimer’s Disease_x0001_ DescriptionA progressive dementia (global cognitive decline) of middle and late life._x0001_ DiagnosisNo one test is diagnostic. It is a clinical diagnosis/diagnosis of exclu-sion. Clinical, abnormal mental status exam and exclusion of otherillnesses (e.g., normal pressure, hydrocephalus, metabolic disease,multi-infarct dementia, tumor, and infections). Etiology is unknown,but frequency increases with age. Familial associations with amyloidprecursor protein and presenilin protein mutations; inheritance ofE4 allele apolipoprotein E. MRI demonstrates cortical atrophy. Sin-gle photon-emission computed tomography (SPECT), PET scanshave bilateral temporoparietal hypometabolism._x0001_ PathologySenile plaques (dystrophic neurites surrounding an amyloid core)and neurofibrillary tangles are prominent, associated with cerebral atrophy and ventricular dilatation.

Hint 354

_x0001_ Treatment StepsSymptoms such as agitation and depression are treatable. Acetyl-cholinesterase inhibitors (tacrine, donepezil, rivastigmine, galantamine). Newer medications include memantine (Namenda).

Front 355

_x0001_ SymptomsProminent, early personality change, apathy, abulia, disordered speech, aphasia.

Back 355

Pick’s Disease_x0001_ DescriptionDementia with lobar atrophy._x0001_ DiagnosisOccasionally familial. CT/MRI—prominent symmetric/asymmetricfrontotemporal atrophy_x0001_ PathologyFrontotemporal lobar atrophy. Argyrophilic neuronal (Pick) inclu-sion bodies in frontal and temporal lobes. Frontal and temporal at-rophy sparing superior temporal gyrus.

Hint 355

_x0001_ Treatment StepsSupportive treatment for dementia.

Front 356

_x0001_ SymptomsDementia. Clinical features determined by location1)(location?)psychomotor slowing, decreased atten-tion, concentration and memory deficits, gait disorder (lower half parkinsonism)2)(location?) aphasia, apraxia, visuospatial defects, amnesia_x0001_ DiagnosisProgressive intellectual decline. Associated stroke risk factors andmultiple infarctions, ventricular dilatation. Multifocal decreases incerebral blood flow on PET/SPECT.

Back 356

Multi-infarct Dementia_x0001_ DescriptionEpisodic neurologic dysfunction secondary to infarcts of the cere-bral hemispheres leading to dementia.1)=subcortical 2)=cortical

Hint 356

_x0001_ Treatment Steps1. Aspirin, ticlopidine, clopidogrel.2. Treat hypertension.

Front 357

_x0001_ SymptomsUrinary incontinence, dementia, gait disturbance (slow, short steps;unstable)._x0001_ DiagnosisNormal CSF pressure. Enlarged cerebral ventricles, relatively normalcortical gyri on CT/MRI. Subependymal CSF resorption on MRI.

Back 357

Hydrocephalus (Normal Pressure)_x0001_ DescriptionProgressive dementia usually occurring in the elderly_x0001_ PathologyIncreased resistance to arachnoid villus absorption of CSF. Associ-ated with subarachnoid hemorrhage, trauma, tumor, infection.

Hint 357

_x0001_ Treatment StepsVentriculoperitoneal shunt. Significant improvement w/ CSF removal.

Front 358

_x0001_ SymptomsSubacute progressive dementia, myoclonus._x0001_ DiagnosisClinical, EEG high-voltage, triphasic periodic complexes on depressed background.

Back 358

Creutzfeldt–Jakob Disease_x0001_ DescriptionProgressive dementia, due to abnormal isoform of prion protein(PrPSc). Disease may be infectious, inherited, or sporadic._x0001_ PathologySpongiform change (vacuolar dilatation of neurons), amyloidplaques, loss of neurons, and gliosis.

Hint 358

_x0001_ Treatment StepsNone.

Front 359

_x0001_ SymptomsPtosis, miosis, anhidrosis, enophthalmos, narrowing palpebral fis-sure, flushing on affected side of face

Back 359

Horner Syndrome_x0001_ PathologyInterruption of the unilateral sympathetic system due to trauma,lung apex tumor, CNS lesions, vascular headache._x0001_ DiagnosisCocaine and para-OH-amphetamine tests

Front 360

_x0001_ SymptomsUnilaterally dilated pupil with slow response to light and accommo-dation; areflexia may be present.

Back 360

Adie’s Pupil_x0001_ PathologyPostganglionic parasympathetic lesion._x0001_ DiagnosisWeak pilocarpine solution results in Adie’s pupil contraction

Front 361

_x0001_ SymptomsVery small pupils that fail to constrict to light with accommodationpreserved. One or both eyes affected

Back 361

Argyll–Robertson Pupil_x0001_ DiagnosisArgyll–Robertson pupil is a sign of neurosyphilis. Rule out CNS structural lesions

Front 362

_x0001_ SymptomsPupils fixed and dilated, ophthalmoplegia and contralateral hemi-paresis

Back 362

Uncal Herniation Syndrome

Front 363

_x0001_ SymptomsDefective direct light reflex with intact consensual reflex on “swing-ing flashlight test.”

Back 363

Marcus Gunn Pupil

Front 364

_x0001_ SymptomsEye “down and out.”

Back 364

Third Cranial Nerve LesionAffects medial rectus, superior rectus, inferior rectus, inferioroblique, and levator of eyelid.

Front 365

_x0001_ Symptomsvertical diplopia.

Back 365

Fourth Cranial Nerve LesionSuperior oblique muscle affected;

Front 366

_x0001_ SymptomsWeak lateral rectus, poor abduction

Back 366

Sixth Cranial Nerve Lesion

Front 367

Unreactive, Midposition Pupil (lesion localization)

Back 367

Midbrain lesion

Front 368

Pinpoint Pupils

Back 368

Pontine lesion

Front 369

Unilaterally Dilated and Unreactive Pupil

Back 369

Possible third nerve lesion

Front 370

—Daytime sleep attacks accompanied by cataplexy,hypnogogic hallucinations, and sleep paralysis. Rapid onset REMsleep.

Back 370

Narcolepsy

Hint 370

Treat with amphetamine, pemoline, methylphenidate,dextroamphetamine. Clomipramine for cataplexy.

Front 371

—Arousal from NREM sleep

Back 371

Night Terror

Front 372

—Awakening from REM sleep

Back 372

Nightmare

Front 373

Gliomas typemost common of all gliomas, and most commonbrain tumor in childhood

Back 373

Astrocytoma

Front 374

Gliomas typeusually frontal lobe, slow growing, presentswith headache, seizures, and the tumor may bleed.

Back 374

Oligodendroglioma

Front 375

most common posterior fossa tumor in chil-dren. Fast growing, radiosensitive

Back 375

Medulloblastoma

Front 376

Gliomas typeInfratentorial morethan supratentorial and filum terminale

Back 376

Ependymomaependymal surface location

Front 377

CNS neoplasm typeUsually benign, associated with type 2 neurofibromatosis

Back 377

Meningiomas

Front 378

CNS neoplasm typeSuprasellar, visual field defects often (bitemporal hemianopsia), en-docrinopathies, diabetes insipidus.

Back 378

Craniopharyngiomas

Front 379

CNS neoplasm typeEndocrine and visual symp-toms

Back 379

Pituitary TumorsSecretory in 75%, nonsecretory in 25%

Front 380

CNS neoplasm typeUnilateral hearing loss, tinnitus

Back 380

Acoustic SchwannomaMay compress cranial nerves V, VII,and brain stem. Bilateral in neurofibromatosis type 2

Front 381

_x0001_ SymptomsLucid interval after brief unconsciousness followed by increasingobtundation. Sometimes no lucid interval present. Extremeheadache, contralateral hemiparesis

Back 381

Epidural Hematoma_x0001_ DiagnosisHistory and physical, CT scan.

Hint 381

_x0001_ Treatment Steps1. Neurosurgical evaluation for possible drainage.2. Empiric anticonvulsants.3. May use mannitol to control intracranial pressure/swelling

Front 382

Acute, subacute, and chronic from cortical vein tear.Acute—From high speed trauma, coma from impact; CT useful(see Fig. 11–2).Subacute—Several days of lethargy, then deterioration; MRI.Chronic—Minor trauma may cause gradual deterioration; MRI.

Back 382

Subdural Hematoma

Front 383

_x0001_ SymptomsSudden-onset severe headache, may have sentinel bleed with minorsymptoms. May have stiff neck, photophobia, nausea, and focal signs

Back 383

Subarachnoid Hemorrhage

Hint 383

_x0001_ Treatment Steps1. Supportive care.2. Bed rest, analgesics.3. Prophylactic anticonvulsants.4. Carefully control blood pressure.

Front 384

_x0001_ SymptomsHigh fever, muscular rigidity, akinesia, decreased consciousness, au-tonomic dysfunction all as a complication of major tranquilizers, tri-cyclic antidepressants, or withdrawal from dopaminergic agents.

Back 384

Neuroleptic Malignant Syndrome (NMS)

Hint 384

_x0001_ Treatment Steps1. Withdraw neuroleptics.2. Bromocriptine or dantrolene.3. Supportive care.

Front 385

_x0001_ SymptomsAcute respiratory failure in a patient with myasthenia gravis.

Back 385

Myasthenic Crisis

Hint 385

_x0001_ Treatment Steps1. Discontinue cholinesterase (ChE) inhibitors.2. Ventilate patient in intensive care unit (ICU).3. Slowly reintroduce ChE inhibitors.

Front 386

_x0001_ SymptomsDepression of level of consciousness with myoclonus, asterixis,tremor, seizures. EEG abnormal; may have triphasic waves.

Back 386

Uremic Encephalopathy

Hint 386

Treat renal disease.

Front 387

_x0001_ SymptomsConfusion, lethargy, headache, seizures. The more rapid the sodium drop, the more severe the symptoms.

Back 387

Hyponatremia

Hint 387

Syndrome of inappropriate an-tidiuretic hormone (SIADH): treat with water restriction; demeclocycline if chronic.

Front 388

_x0001_ SymptomsAbdominal pain, vomiting, constipation or diarrhea, confusion, seizures, neuropathy._x0001_ DiagnosisWatson–Schwartz test for elevated aminolevulinic acid

Back 388

Acute Intermittent Porphyria_x0001_ PathologyDeficiency of porphobilinogen deaminase

Hint 388

_x0001_ Treatment Steps1. Hematin and high-carbohydrate diet.2. Carbamazepine for seizures.

Front 389

_x0001_ SymptomsAcute exposure—abdominal colic, headache, behavioral change, en-cephalopathy, seizures. Chronic exposure—gastrointestinal distur-bances, anemia, weight loss, behavioral disturbances, cognitive impairment. Peripheral neuropathy (wrist drop) in adults.

Back 389

Lead Toxicity_x0001_ DiagnosisBasophilic stippling, lead line on x-ray. Lead colic is most frequentsign in adults. Screen with lead level, ethylenediaminetetraaceticacid (EDTA) test if lead level not over 80._x0001_ PathologyNeuropathy from segmental demyelination.

Hint 389

_x0001_ Treatment StepsChelation with Ca-EDTA or penicillamine.

Front 390

_x0001_ SymptomsAsterixis, slow EEG, depressed mental status, elevated blood ammo-nia.

Back 390

Liver Disease—Hepatic Encephalopathy

Hint 390

Give protein-free diet, neomycin, or lactulose.

Front 391

_x0001_ SymptomsNausea, vomiting, abdominal pain, renal failure, neuropathy, encephalopathy._x0001_ DiagnosisHistory, exam, Mees’ lines (transverse lines in nails).

Back 391

Arsenic Toxicity

Hint 391

_x0001_ Treatment StepsUse dimercaprol (BAL) or penicillamine.

Front 392

—Wernicke’s encephalopathy, nystagmus,ataxia, confusion, amnesia

Back 392

Thiamine (B1) deficiency

Front 393

—Pernicious anemia, megaloblastic ane-mia, subacute combined spinal cord degeneration

Back 393

Cobalamin (B12) deficiency

Front 394

—Excess can produce sensory neuropathy

Back 394

Pyridoxine (B6)

Front 395

_x0001_ SymptomsTinnitus, hearing loss, delirium, coma, seizures

Back 395

Salicylate Toxicity_x0001_ DiagnosisHistory, respiratory alkalosis, serum salicylate level, rapid screen: ferric chloride test

Hint 395

_x0001_ Treatment Steps1. Treat shock.2. Protect airway.3. Routine drug intoxication measures.

Front 396

_x0001_ SymptomsVomiting, lethargy, and delirium due to brain edema after a viral ill-ness that was treated with aspirin, with abnormal liver functions, hy-poglycemia, and respiratory alkalosisLiver shows microvesicularfatty infiltration

Back 396

Reye’s Syndrome

Front 397

_x0001_ SymptomsType I—visceromegaly. Type II/III—gaze palsies, trismus, spasticity,dementia, seizures, and visceromegaly.

Back 397

Gaucher’s Disease_x0001_ DescriptionGlucocerebroside lipidosis._x0001_ DiagnosisClinical. Bone marrow may contain Gaucher cells (lipid-ladenmacrophages). Enzymatic analysis._x0001_ PathologyDeficiency of lysosomal glucocerebrosidase. Autosomal recessive.

Front 398

_x0001_ SymptomsPolyneuropathy with neuralgia, cerebrovascular disease in middleage, vasculopathy with renal and cardiac disease, cutaneous angio-keratoma and telangectasias.

Back 398

Fabry’s Disease_x0001_ DescriptionSphingolipidosis. Inborn error of metabolism._x0001_ DiagnosisClinical exam. Enzymatic analysis._x0001_ PathologyDeficiency of lysosomal α-galactosidase A. Sex-linked recessive. Gly-cosphingolipid deposition in tissues (eyes, kidney, heart, CNS).

Hint 398

Treatment StepsCarbamazepine, phenytoin for pain. Renal transplantation.

Front 399

_x0001_ SymptomsProgressive dementia and visual impairment, irritability, muscleweakness, spasticity, seizures._x0001_ DiagnosisCherry-red spot in the fovea. Abnormal electroretinogram (ERG) and visual evoked potential (VEP).

Back 399

Tay–Sachs Disease_x0001_ DescriptionInfantile cerebromacular degeneration caused by mutations of α-subunit of the lysosomal β-hexosaminidase A gene._x0001_ PathologyAccumulation of gangliosides in retina and CNS neurons. Autosomal recessive

Front 400

_x0001_ SymptomsPain, fatigue, and stiffness on exertion._x0001_ DiagnosisForearm exercise test—low/absent lactate production. Elevatedmuscle glycogen on biopsy.

Back 400

McArdle’s Disease_x0001_ DescriptionA glycogen-storage disorder due to a mutation in the myophosphorylase gene._x0001_ PathologyDeficient muscle phosphorylase

Hint 400

_x0001_ Treatment StepsGlucose and reduce exercise.

Front 401

Progressive weakness,hypotonia, heart failure

Back 401

Pompe’s DiseaseAcid α-glycosidase (acid maltase) deficiency

Front 402

Episodic Muscle Weakness, low potassium

Back 402

Episodic Muscle WeaknessFamilial hypokalemic periodic paralysis—autosomal dominant,due to mutation of DHP-sensitive calcium channel

Front 403

Episodic Muscle Weakness, elevated potassium.

Back 403

Familial hyperkalemic periodic paralysis—autosomal dominant(mutation of the human muscle sodium channel), shorter weakness attacks

Front 404

Obesity, mental retardation, retinitis pigmentosa, hypogonadism,polydactyly, diabetes insipidus, autosomal recessive

Back 404

Laurence–Moon–Biedl Syndromelooney,moon,blind

Front 405

Multisystem atrophy with orthostatic hypotension and CNS degeneration (parkinsonism; cerebellar, pyramidal features)

Back 405

Shy–Drager SyndromeNeuronal loss intermediolateral cell column

Front 406

Most common spinocerebellar degeneration onset childhood. Mutation in GAA repeat frataxin (X25) gene

Back 406

Friedreich’s Ataxia

Front 407

Demyelinating polyneuropathy, slowly progressive, peroneal muscleatrophyMutation in peripheral myelin protein-22 gene.

Back 407

Charcot–Marie–Tooth Disease

Front 408

Café au lait spots (more than six of 1.5-cm size), neurofibromas, schwannomas, optic nerve gliomas,Lisch nodules iris.

Back 408

Neurofibromatosis 1mutation in NF-1 neurofibromin gene

Front 409

Bilateral vestibular schwannomas, menin-giomas, astrocytomas, posterior lens opacities

Back 409

Neurofibromatosis 2mutation in NF-2(MERLIN protein) gene.

Front 410

mental retardation, epilepsy, cutaneous faciallesions, and organ hamartomasAutosomal dominant

Back 410

Tuberous Sclerosis

Front 411

Autosomal disorder with retinal and cerebral hemangioblastomas;renal, pancreatic, and epididymal cysts; and renal carcinomas

Back 411

von Hippel–Lindau Disease

Front 412

Progressive cerebellar ataxia (Purkinje cell degeneration), oculocu-taneous telangiectasia, radiosensitivity, immunodeficiency and lym-phoid malignancies.

Back 412

Ataxia–TelangiectasiaDue to mutated ATM gene with phosphoinositol-3′kinase activity

Front 413

_x0001_ DescriptionStatic encephalopathy with abnormal motor function from birth.Antepartum events cause 90%; also associated with prematurity andlow birth weight.

Back 413

Cerebral Palsy_x0001_ DiagnosisHistory and physical examination, skull x-ray, CT/MRI of the head,EEG, and psychological testing, evaluation of developmental mile-stones._x0001_ PathologyIncludes periventricular leukomalacia, periventricular/intraventric-ular hemorrhages, infarction

Hint 413

_x0001_ Treatment Steps1. Multidisciplinary support.2. Orthopedic intervention.3. Physical/occupational therapy.4. Control seizures.5. Social services.

Front 414

Cerebral Palsyassociated with prematurity. Either periventricularleukomalacia or periventricular hemorrhage (greater involvement of intellectual function)

Back 414

Spastic diplegia

Front 415

Cerebral Palsyassociated with congenital malformations & intrauterine infections. Severe disability associated with mental retardation and seizures (Lennox–Gastaut syndrome)

Back 415

Spastic quadriplegia

Front 416

Cerebral Palsycaused by developmental malformations, stroke, trauma. Seizures associated

Back 416

Spastic hemiplegia

Front 417

Cerebral Palsybilirubin encephalopathy (rare) and causes of spasticquadriplegia

Back 417

Athetosis

Front 418

_x0001_ Symptomsshort seizure without focal features_x0001_ DescriptionSeizure in child age 3 months to 5 years, associated with fever/infection

Back 418

Febrile Seizures_x0001_ DiagnosisHistory and physical exam; rule out meningitis, septicemia. Hospitaladmission, including routine lab, lumbar tap._x0001_ PathologyUnknown.

Hint 418

_x0001_ Treatment Steps1. Temperature reduction (tub bath, acetaminophen [Tylenol]).2. Medication (diazepam [Valium] 0.2 mg/kg rectally or IV).

Front 419

_x0001_ SymptomsAsymptomatic, or may demonstrate pain, red eye, and vision loss.May note halos around lights.

Back 419

Glaucoma_x0001_ DescriptionOphthalmic disorder of elevated intraocular pressure, which is etiology of 10% of blindness in the United States._x0001_ DiagnosisOn exam, elevated intraocular pressure (over 22 mm Hg by Schiøtz’tonometry)_x0001_ PathologyTypes include primary angle-closure, open-angle, secondary, andcongenital. May be of sudden obstructive (primary angle-closure) etiology, or chronic obstruction (open-angle).

Front 420

eye pain, vomiting, visionloss, sudden onset

Back 420

Primary angle-closure GLAUCOMA

Hint 420

_x0001_ Treatment StepsPrimary Angle-Closure—Surgical iridectomy, with acetazo-lamide (Diamox) and β-blockers preop.

Front 421

vision field defects, disccupping, no pain!

Back 421

Primary open-angle GLAUCOMA

Hint 421

_x0001_ Treatment StepsPrimary Open-Angle—Treatment includes topical (eyedrops):• β-Blockers––Timoptic (timolol).• Carbonic anhydrase inhibitors––Trusopt(clorzolamide), Diamox(acetazolamide).

Front 422

_x0001_ SymptomsNarrowed visual field; larger blind spot, vision may be normal or im-paired._x0001_ DiagnosisFundoscopic exam (disc swollen, associated hemorrhages/exu-dates).

Back 422

Papilledema_x0001_ DescriptionElevation/swelling of optic nerve head.Papilledema may cause optic atrophy._x0001_ PathologySecondary to elevated CSF pressure, and a result of infection, opticneuritis, metabolic disease, CNS lesions.

Hint 422

_x0001_ Treatment StepsTreat primary cause.

Front 423

_x0001_ Symptoms/DiagnosisProgressive painless visual loss, or asymptomatic. Diagnose via oph-thalmoscopic examination._x0001_ DescriptionLens opacity (nuclear, cortical, and subcapsular).

Back 423

Cataract_x0001_ PathologyAge related; ultraviolet light exposure association, and may also relate to trauma, corticosteroids, and diabetes.

Hint 423

_x0001_ Treatment StepsCataract removal and intraocular lens implantation.

Front 424

light flashes in eye

Back 424

Retinal detachmentretinal degeneration ortrauma induced

Front 425

Constricted pupil differential

Back 425

iritis, drugs, Horner’s

Front 426

Dilated pupil differential

Back 426

Adie’s, glaucoma, drugs, third nerve lesion.

Front 427

thickened conjunctiva

Back 427

Pinguecula

Front 428

thickened conjunctiva encroaching on cornea

Back 428

Pterygium

Front 429

small pupil, ciliary injection

Back 429

Iritis

Hint 429

treat with cycloplegics andsteroids

Front 430

large pupil, diffuse injection

Back 430

glaucoma

Hint 430

treat with pilocarpine, acetazolamide [Diamox], etc.

Front 431

eye anterior chamber blood

Back 431

Hyphema—trauma induced

Front 432

blocked meibomian gland duct

Back 432

Chalazion

Front 433

Sudden vision loss

Back 433

rule out artery (secondary to emboli, retinawhite) or vein occlusion.

Front 434

xanthomas and hepatomegaly?

Back 434

- primary biliary sclerosis- other sx: pruritis- lab: increased alk phos, cholesterol, IgM- associated with Sjogrens, Raynauds, scleroderma, autoimmune hypoTH, celiac, increased malignancy- tx: ursodeoxycholic acid, only def tx = liver transplant

Front 435

- anti-smooth muscles- anti-smith- pANCA

Back 435

- acute and chronic hepatitis- SLE (sensitive but only 30-50%)- Churg-Strauss, micrscopic polyangitis

Front 436

pt with hep C?

Back 436

- all pts should receive vaccine for hep A, B including during pregnancy

Front 437

pregnant pt with HCV?

Back 437

- OK to breast feed, vaginal delivery, sex without barrier protection if in stable relationship

Front 438

cholecdochal cyst

Back 438

- congenital abnormality of biliary ducts => dilation of intra/extra hepatic biliary ducts- infants: juandice, acholic stools; kids - abd pain, jaundice, recurrent pancreatitis; adults: vague pain, cholangitis- US -> CT -> MRI- can become choriocarcinoma

Front 439

baby with jaundice, acholic stools?

Back 439

- biliary atresia, choledocal cyst

Front 440

carolis syndrome

Back 440

- congenital d/o, intrahepatic dilation of bile ducts

Front 441

pancreatic pseudocyst occurs where?

Back 441

- as retroperitoneal mass

Front 442

ddx peritoneal fluid

Back 442

- portal HTN, trauma, infx, pancreatitis, malignancy- to ddx need to know exudate vs transudate => calculate SSAG = ascites albumin - serum albumin => if >1.1 = transudative = portal HTN

Front 443

signs of decreased liver synthetic fx?

Back 443

- decreased serum albumin, increased INR

Front 444

what PEX is not associated with hyperaldo?

Back 444

- will see decreased Na but should not see EDEMA (b/c then something else)

Front 445

pt with newly dx cirrhosis?

Back 445

- do screening endoscopy to eval esoph varices => if + give beta blocker

Front 446

octreotide

Back 446

- used for tx hepatorenal syndrome

Front 447

unconjugated hyperbili

Back 447

- unconjugated bili > 90% of T bili- estimate Hg and periph smear to check for hemolysis

Front 448

pt with chronic hep C but normal LFTs x 1 yr

Back 448

- no tx needed

Front 449

when to check for hep B and C in pts with hx of blood transfusion?

Back 449

- hep B: prior to 1986- hep C: prior to July 1992

Front 450

when to check HCV?

Back 450

- IV drug, blood transfusion/transplant prior July 1992, HD, chronically elevated ALT, children born to HCV mom

Front 451

when to check HBV?

Back 451

- hyperendemic areas (AFrica, SE asia, ME, Amazon, Haiti, Dominican Republic), male + male, IVDA, dialysis, HIV+, pregnant, contacts of HBV pts

Front 452

liver toxins?

Back 452

- dose dependent direct liver toxins: carbon tetrachloride, acetaminophen, tetracycline, amonita phalloides- idiosyncratic rxn: isoniazide, chlorpromazine, halothane, antiretrovirial

Front 453

drug induced liver dz?

Back 453

- cholestasis: chlorpromazine, nitrofurantoin, erythromycine, anabolic steroids- fatty liver: tetracycline, valproate, anti-retrovirals- hepatitis: halothane, phenytoin, isoniazide, alpha-methyldopa- toxic/fulminant liver dz: carbon tetrachloride, acetaminophen- granulomatous: allopurinol, phenylbutazone

Front 454

labs on alcoholic hep?

Back 454

- AST:ALT >2

Front 455

biopsy of hepatitis?

Back 455

- panlobular mononuclear infiltratio nwith hepatic cell necrosis- if negative serology then consider drug induced

Front 456

OCP on liver?

Back 456

- abnormal LFTs but no change in biopsy

Front 457

dx of autoimmune hep?

Back 457

- consider once r/o all possible causes of drug or viral- see +ANA, smooth muscle ab

Front 458

wilson's dz?

Back 458

aka hepatolenticulo degeneration- sx <30y.o., cirrhosis, neuropsych sx (parkinson, mood), kayser fleischer rings- decreased creuloplasmic => decreased Cu excretion => deposits in lier, basal ganglia, cornea- associated with Fanconi's dynrome, hemolytic anemia, neuropathy- dx: liver biopsy => hepatic Cu level > 250mcg/gram dry weight, or low ceruloplasmi + high urinary Cu excretion or K-F rings

Front 459

hemochromatosis

Back 459

- abnormally high iron abosroption => liver disease, pigmentation, DM, impotence, arthropathy

Front 460

gallbladder Ca

Back 460

- RF: southwest native american, mex-america, chronic gb inflammation, hx gallstones, porcelain gallbladder, salmonella typhi, anatomic variation- very rare

Front 461

pregnant +HBV

Back 461

- if active can tranmit to baby via placenta or during delivery esp if dvlped during 3rd trimester- + HBsAG, HBeAg, IgM, anti-HBcAb- if HBeAg negative then risk decreases from 95% to 20%- baby's risk of chronic hepB = 90%, thus give passive immunization with HBIG and active HBV vaccine

Front 462

Pancreatic RF

Back 462

- smoking, chornic pancreatitis, fhx, DM, obesity, hgih fat diet- ALCOHOL is not RF

Front 463

pt with severely elevated AST, ALT, mild change in PT, albuin

Back 463

- hepatocellular pattern injury most likely 2/2 med; e.g. pt with headahces => most likely using acetaminophen though don't say in stem- it increased PT and low albmin, think cirrhosis

Front 464

pt with pancreatitis sx?

Back 464

- do U/S, most likely 2/2 gallstones- don't do CT- only do CT when tx doesn't work

Front 465

sx of chronic liver dz?

Back 465

- weight loss, gynec, test atrophy, impotence 2/2 hyperE (low SHBG)

Front 466

pt with cirrhosis now with asterixis, confusion, reversal sleep cycle?

Back 466

- hepatic encephalopathy 2/2 increase ammonia in blood b/c can't detox to urea- increased sensitivity to GABA, false NT production- precipitating factors: increased protein diet, alkalosis, diuretic therapy, high volume paracentesis, portocaval shunts- not caused by increased urea!

Front 467

chronic HBV infx?

Back 467

- HBsAg for > 6 months - do livery biopsy to assess hepatic injury- if liver damage = chronic active, if no liver damage = chronic persistance

Front 468

post cholecystectomy pain?

Back 468

- sphincter of oddi dysfx:- sx: RUQ pain, increased LFTs during attack; do oddi manometry, see increased pressure; tx: sphincterotomy- dx of exclusion = functional pain

Front 469

edema in cirrhosis?

Back 469

- 2/2 decreased protein => indecreased intravascular oncotic pressure

Front 470

types of gallstones

Back 470

1. cholesterol, 2. pigment (calcium bilirubate) 3. mixed- 80% = cholesterol and mixed = radiolucent

Front 471

pregnant and cholecystitis?

Back 471

- repeated attacks =? cholecystecty in 2nd trimester- else give ursodeoxcholic acid to dissolve stones that will return once stop tx

Front 472

travel, RUQ pain, dysentary, single cyst in right lobe liever

Back 472

- AMEBIC livery cyst, histolyticia, cyst aspiraition = sterile, acellular, anchovy paste- usually invades colon => bloody diarrhea- tx: metronidazole

Front 473

dx liver cyst

Back 473

- amebic cyst- pyogenic liver bascess: severe presentaiton, 2nd to surgery, GI infx, acute appendicitis, tx broad spectrum abx = ceftriaxone- hydatid cyst - echinococcus granulose = dog contact- cystic ca= thick ,irregular, hpervascular wall, numerous septate

Front 474

acalulous cholecystis

Back 474

- GB inflammation without gallsontes, 2/2 extensive burns, trauma, prlonged TPN, fasting, mechanical ventilation

Front 475

tx of gallstone pancreatitis?

Back 475

- tx pancreatitis, then do cholecystitis

Front 476

signs of met to liver?

Back 476

- suggestion of GI malignancy (+occult blood), anemia 2/2 GI leed, firm hepatomegaly, increased alk phos more than increase in ast, alt = ca infiltration rather than liver injury- pleural effusion of L; note if on Rthen may be 2/2 hdrothorax = cirrhosis

Front 477

post op cholestasis

Back 477

- after major surgery 2/2 hypotension, blood loss into tissues, blood transfusion- increased pigment load from transufion, decrased liver function, decreased renal bilirubin excretion- high bili, alk phos

Front 478

halothane

Back 478

- anesthetic causes hepatotox, not used anymore

Front 479

increased risk of alcohol liver injury?

Back 479

- women > men

Front 480

non-alcoholic fatty liver dz?

Back 480

- associated with obesity, DM II- path: insulin resistance => increased at in liver => increased lipolysis => increased insulin levels- dx: biopsy- note: decreased glycogen synthesis in liver in DM II, but increased glucagon

Front 481

increase in alk phos?

Back 481

- check GGT- if high = liver- if low = other like bone

Front 482

pt with mildly elevated LFTs on routine exam?

Back 482

repeat in 6 months, if again increased then = chronic and do viral, hemochromatosis, fatty liver testing- if those are negative then test for muscle d/o polymyositis, thyroid dz

Front 483

most important test of liver fx?

Back 483

- PT! b/c all clotting factors synthesized by liver- don't interpret LFTs b/c can go down 2/2 recovery or fewer hepatocytes

Front 484

left sided pleural effusion

Back 484

pancreatitis, maligancy

Front 485

dx of alpha 1 antitrypsin?

Back 485

measure alpha one in serum => then confirm with genetic testing- testing is indicated in all premature chronic bronchitis, emphysema, dyspnea, non-smokers with COPD- tx: purified A1AT- test relative of homozygouses

Front 486

mallory bodies

Back 486

alcoholic hepatitis but is not diagnositic and not used for dx

Front 487

vanishing bile duct syndrome

Back 487

primary biliary cirrhosis, not primary sclerosing cholangitis

Front 488

hbv tx

Back 488

indications: persistance increased alt, detectable serum hbsag, hbv dna- alt is most important predictor of response to tx; BEST is 2x normal- tx: alpha interferon or lamivudine

Front 489

hep A vs hep B vs hep C

Back 489

- hep A: flu like, jaundice, dark urine, dirty place, other people with same sx- hep b, sx 1-6 mo s/o infx- acute hep C: asympt

Front 490

serologic makers of hbv?

Back 490

- hbsAg = 1st serologic marker, always dectable as long as infected- window period = period between hbsag undetected and anti-hbs undetected-anti-hbc= second serologic marker, makes IgM and IgG, IgM is present during window period- HbeAg = viral replication and infectivity, if >3mo then increased risk chronic

Front 491

+bilirubin in dipstick?

Back 491

- hyperbili 2/2 conjugated bili and not unconjugated (not water soluble)

Front 492

rotor syndrome

Back 492

- benign defect of hepatic storage of conjugated bili => leak into plasma, normal LFTs

Front 493

hep C tx

Back 493

indications: natural hx of dz, stage, liver biopsy, lfts, + hcv rna- if mild, tx is interferon- if medium e.g. increased alt, hcv rna+, chronic hep = tx with interferon and ribavirin (lamivudine is for hepb)

Front 494

anaphylaxis to blood transufsions?

Back 494

IgA deficiency

Front 495

gilbert dz?

Back 495

- decreased udp glucuronl tranferase => unconjugated hyperbili

Front 496

crigler-najjar type i

Back 496

- jaundice, neuro impairment, kernicterus (bilirubin enceph), increased indirect bili, normal LFTs- tx Liver tx, meanwhile light therapy

Front 497

Crigler-Najjar type 2

Back 497

- milder, survive into adulthood, no kernicterus- tx phenobarbital as needed

Front 498

complications of pancreatitis?

Back 498

1. hypovolemic shock: inflammatory factors => increased vascular permeability => fluid in retroperitoneum => need several L of fluid2. LV failure 2/2 vascular volume loss3. cardiac tamponade4. pseudocyst, asympt unless rupture, hemorrhage or infx5. retroperitoneal hemorrhage => see flank or umbilical ecchymoses

Front 499

tx PBC?

Back 499

- ursodeoxycholic acid, slows dz progression, reduces sx- if advanced then tx is liver transplant (eg. cirrhosis, liver damage)- 7-10 yr survival after 1st sx- symptomatic tx = cholestyramine for itching relief

Front 500

intrahepatic cholestasis of pregnancy? vs normal physiologic changes? PBL?

Back 500

- cholestatsis: 2nd, 3rd trimester => increased bile acid 2/2 genetic or hormone; see increased ALT, AST, alk phos, serum bile; must r/o viral hepatitis; dx of exclusion; tx: ursodeoxycholine, cholestyramine not as effective and SE- normal = increased alk phos, nl bili, alt, ast, ggt- PBL - see xanthomas

Front 501

extrahepatic copmlications of hepC?

Back 501

cryoglobulinemia => membranous GN, B-cell ly,mphoma (not T), plsmacytoses, AI dz e.g. sjogren, thyroiditis, lichen planus, porphyria cutanea tarda, ITP

Front 502

reye's syndrome

Back 502

- aka fatty liver with encephalopathy- kid with infx, takes salicylate => mito injury => hypoglycemia, liver failure, cns damage- liver bx: fatty vacuolation without inflammation- tx glucose, ffp, mannitol- THUS ASA IS C/I IN KIDS

Front 503

path of:acute etoh hepatitis, acute viral hepatitis, chronic active viral hepatits, PBC

Back 503

- etoh: balloon degeneration with polymorphic (neu, mono, lymph) infiltrate- acute viral hep: panlobular monoulear infiltrate with bridging necrosis- chroinc: piecemeal necrosis- PBC: inflammatory granulomatous destruction of biliary ducts

Front 504

emphysematous cholecystitis

Back 504

infx GB wall by gas forming bacteria - clostridium, escherichia, staph, strep,. pseudo, kleb - increased risk from vascular problems, immunosuppression (DM), gallstones - sx: RUQ, N/V, crepitus - KUB shows air fluid in gallbladder; U/S: curvilinear gas shadowing - tx: cholecystectomy, abx against clost (zosyn or amp-sublactam)

Front 505

acute cholangitis

Back 505

- charcot's tirad: RUQ pain, jaundice fever- biliar tract obstruction => bact infx

Front 506

pancreatic pseudocyst

Back 506

- fake cyst b/c no epithelial lingin, fibrous capsuel- contains inflammatory fluid: amylase, lipase, enterokinase- tx if persists > 6wks = drain

Front 507

primary sclerosis cholangitis

Back 507

- onion skin pattern stricturing of ducts- complications = biliary stricture, cholangitis, cholelithiasis, cholangiocarcinoma, CRC- associated with UC, see high HLA-B8, IgM, pANCA- dx via cholangiography => beading pattern, U/S and biopsy aren't useful- tx: ursodeoxycholate, dilation, stenting- Liver transplant else life span 12 yrs

Front 508

hydatid cyst tx

Back 508

- 2/2 echinococccus- surgical resection under albendazole- don't aspiration else anaphylaxis

Front 509

cysticercosis

Back 509

- infx by tenia solium => brain, muscle

Front 510

dubin-johnson syndrome

Back 510

- black liver- conjugated bilirubin, sephardic jews- trigger: pregnancy, ocp- urine: Nl urine coproporphyrin but 80% is type I vs type III- normal LFT is requirement for dx- no tx

Front 511

black liver

Back 511

dubin johnson

Front 512

pt with chronic hepatitis and cirrhosis now with weight loss?

Back 512

- first step in eval is check for tumor marker AFP- some imaging must be done b/c neg AFP doesn't rule out- checking ascite fluid is useless

Front 513

pt with hydrothorax?

Back 513

- first do therapeutic thoracentesis, salt restriction, diuretics- if those don't work then do TIPS- don't do portosytemic shunt b/c increased morbidity

Front 514

pt on INH

Back 514

- will have small increase in ALT, AST which is OK- if sx of hepatitis 2/2 iNH stop INH immediately

Front 515

primary liver Ca

Back 515

- HCC: increased AFP, ill defined single lesion - hepatic adneoma- benign, women on OCP, one mass - hepatic angiocarcinome: hx of exposure to vinyl chloride gas, arsenic, thorium, malignant cells line vascular sx

Front 516

What is presentation of sq cell Ca? Where does it hit What is treatment? x3

Back 516

i)nonhealing ulcer ii)the lower lip and below iii)a)excision w/.5-2 cm margins b)nodal dissection if affected c)possible radiation

Front 517

What is interesting about mets of melanoma? what is the timetable like?

Back 517

i)can go anywhere, like muscle of LV ii)not predictable: can be dead in a few months to 20 years b/w resection of primary and metastasis

Front 518

What are sxs of retinal detachment? x2 What is bad prognostic factor?x2 What is intervention and is it an emergency?

Back 518

i)a)floaters b)light flashes ii)a)snow storm in the eye or b)dark cloud at top of visual field: horshoe piece of retina pulled away and can rip out retina at rest. iii)emergency intervention w/laser spot welding

Front 519

What is time line of the 3 kinds of neck masses?

Back 519

i)congenital: have had it for long time, acutely worse ii)inflammatory: days to few weeks, and resolves after few weeks. iii)neoplasm: several months of growth

Front 520

Where is thyroglossal duct cyst? x2 What are they connected to? What is removed in surgery? x3

Back 520

i)a)midline b)level of hyoid ii)tongue iii)a)cyst b)middle of hyoid c)track leading to base of tongue

Front 521

Where are branchial cleft cysts?

Back 521

along anterior edge of SCM, anywhere from in front of tragus to base of neck

Front 522

where is cystic hygroma? What does it feel and look like? What is mandatory b/4 surgery?

Back 522

i)base of neck ii)large, mushy, ill-defined mass occupying entire supraclavicular area, seemingly extending into chest iii)CT b/c may extend into chest

Front 523

What do you do for recently discovered enlarged LNs?

Back 523

usually benign, so complete H and P w/followup in 3-4 weeks. W/u if still there

Front 524

who gets lymphoma? What is presentation? x3 What is first steps? x2

Back 524

i)young people ii)a)multiple enlarged nodes b)low grade fever c)night sweats iii)a)FNA can be done, but b)node removal and give to pathology

Front 525

What is the usual source of metastatic tumor to supraclavicular nodes? How to get dx?

Back 525

i)not from head and neck but below clavicle (lung or intraabdominal tumors) ii)node removal w/pathology

Front 526

Who gets sq cc of mucosae of head and neck? x2 What is diagnostic w/u? What establishes diagnosis and what demonstrates extent? What can be done of the node itself, and what shouldn't be done? Why? what is treatment? x3

Back 526

i)a)men who smoke and drink b)AIDS pts ii)panendoscopy to find primary iii)biopsy of primary; CT shows extent iv)FNA can be done, but open BX of neck mass shouldn't v)incision in neck will interfere w/surgical approach vi)a)resection b)radical neck dissection c)radiotherapy and platinum therapy

Front 527

What are some symptoms of sqCC? x3

Back 527

i)hoarseness ii)persistent painless ulcer on floor of mouth iii)persistent unilateral earache

Front 528

What is presentation of acoustic nerve neuroma? What is best diagnostic modality?

Back 528

i)sensory hearing loss in one ear but not the other ii)MRI

Front 529

what are symptoms of facial nerve tumors? What is best study?

Back 529

i)gradual, unilateral facial nerve paralysis of forehead and lower face (paralysis suddenly=Bells palsy) ii)gadolinium enhanced MRI

Front 530

What are most parotid tumors cell type? Are they benign? What are symptoms of parotid cancer? x2 What can be done to get tissue and what can't? What is the appropriate way to excise/biopsy parotid tumor? Why? What is done for malignant tumors to treat?

Back 530

i)pleomorphic adenoma ii)yes, but malig potential iii)a)hard mass b)painful c)produces paralysis (these don't happen in benign ones) iv)FNA; open BX v)parotidectomy vi)prevents recurrence and spares facial nerve vii)nerve is sacrificed and graft is performed

Front 531

What is the cause of unilateral ENT problems in toddlers? (earache, rhinorrhea, wheezing) What is tx?

Back 531

i)foreign bodies stuck there ii)endoscopy under anesthesia

Front 532

What is ludwig angina and what is the cause? What is the problem with this that is why it is an emergency? What do you do? What may be needed? x2

Back 532

i)abscess of floor of mouth; bad tooth infxn ii)threat to the airway iii)I and D iv)intubate and tracheostomy

Front 533

What do you do for bell palsy?

Back 533

prompt administration of anti-viral meds

Front 534

Do facial nerve injuries due to trauma ever have delayed paralysis? Why do they get it later, and what will happen?

Back 534

i)no: get paralysis immediately ii)if get later, due to swelling and will resolve on own

Front 535

What is symptom of cavernous sinus thrombosis? What is it due to? How to manage? x4

Back 535

i)get diplopia ii)frontal or ethmoid sinusitis iii)a)emergent hospitalization b)IV abx c)CT scans d)drainage of affected sinuses

Front 536

what can you treat epistaxis in kids with? What do kids get it from? 18 y/o? x2 What do you need to do for each of these cases? What is management of elderly and hypertensive getting epistaxis? x2 What is last line therapy?

Back 536

i)phenylephrine spray and local pressure ii)pick nose iii)a)coke b)juvenile nasopharyngeal angiofibroma iv)a)posterior packing b)surgical resection b/c can eat at nearby structure v)a)BP control b)posterior packing vi)surgical ligation of feeding vessels

Front 537

What is diff in dizziness due to inner ear disease vs cerebral disease? What is treatment for each?

Back 537

i)inner ear: room spinning around them ii)brain: unsteady pt but room is perceived to be stable iii)a)meclizine, phenergan, or diazepam b)neurologic w/u