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200 Cards in this Set

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Cushing's syndrome: what is the disturbacne
Increased cortisol die to variety of causes
Cushing's syndrome: what is the number 1 exogenous cause and how will ACTH appear in this case
Exogenous steroids cause low cortisol by suppressing ACTH
Cushing's syndrome: name the 3 most common endogenous causes and the relative incidences 3
1. Cushing's disease (70/100
2. Ectopic ACTH (15/100)
3. Adrenal causes (15/100)
Cushing's syndrome: describe Cushing's disease
This is specifically due to an ACTH secreting pituitary adenoma
Increased ACTH leads to increased cortisol
Cushing's syndrome: describe ectopic ACTH
A nonpituitary tissue making ACTH
Increased ACTH leads to increased cortisol
Cushing's syndrome: what are 2 common causes of ectopic ACTH 2
1. Small cell lung cancer
2. Bronchial carcinoids
Cushing's syndrome: describe adrenal causes of Cushing's syndrome 4
1. Adrenal adenoma
2. Adrenal carcinoma
3. Nodular adrenal hyperplasia
Cortisol is primarily increased and thus ACTH is low
Cushing's syndrome: what are some clinical findings? 10
1. HTN
2. Weight gain
3. Moon facies
4. Truncal obesity
5. Buffalo hump
6. Hyperglycemia due to insulin resistance
7. Thinning and striae in the skin
8. Osteoporosis
9. Amenorhea
10. Immune suppression
Cushing's syndrome: what is dexamethasone and how is it used to dx the cause of Cushing syndrome?
Dexamethasone is a synthetic glucocorticoid.
It is used diagnostically in the dexamethasone supression test (DST) where a patient is given a low and high dose each followed by a cortisol measurement
Cushing's syndrome: what is the normal response to DST?
In a normal patient administered low-dose dexamethasone feeds back negatively and appropriately to the pituitary to supress ACTH
Thus, the normal response after low dose dexamethasone is low cortisol
Cushing's syndrome: what is the Cushing's disease response to DST?
Cushing's disease = ACTH increased due to pituitary adenoma
After low dose - cortisol will still be high like at baseline
After high dose - ACTH supression is achieved and cortisol will be low
Cushing's syndrome: what is the ectopic ACTH response to DST?
Ectopic ATCH producing tumors don't respond to dexamethasone
Therefore, cortisol will remain high after both the low and high dose
Cushing's syndrome: what is the cortisol producing tumor response to DST?
ACTH is not involved in production of cortisol here, so dexamthasone will have no effect
Therefore, cortisol will remain high after both the low and high dose
Hyperaldosteronism: what is Conn's syndrome
Conn's syndrome is the eponym for primary hyperaldosteronism
Hyperaldosteronism: what is a common cause of primary hyperaldosteronism
Aldosterone secreting tumor such as adrenal carcinoma
Hyperaldosteronism: what are the sx of primary hyperaldosteronism 4
1. HTN (salt retention)
2. Potassium wasting (hypokalemia)
3. Proton wasting (metabolic alkalosis)
4. Low plasma renin
Hyperaldosteronism: what is a tx for primary hyperaldosteronism and how does it work?
Spironolactone
Competitive aldosterone antagonist
Hyperaldosteronism: describe secondary hyperaldosteronism
This is where the kidneys think they are being underperfused and so they jack up the renin-angiotensin-aldosterone pathway
Renin is high here
Hyperaldosteronism: what are some causes of secondary hyperaldosteronism 4
1. Renal artery stenosis
2. Chronic renal failure
3. Congestive heart failure
4. Nephrotic syndrome
Addison's disease: what is it
Chronic adrenal insufficiency that is due to adrenal atrophy or destruction
This affects all adrenal cortex layers and so it leads to primary insufficiency of aldosterone and cortisol
Addison's disease: what are some know causes 3
1. Autoimmune
2. Tuberculosis
3. Metastasis
Addison's disease: what are the sx 5
1. Low aldosterone
2. Low cortisol
3. Hypotension (salt-wasting)
4. Hyperkalemia
5. Elevated ACTH leads to skin hyperpigmentation
Addison's disease: why does elevated ACTH cause hyperpigmentation?
POMC is the precursor protein for both ACTH and MSH. So if one is increased, the other is increased.
Addison's disease: how would you differentiate this from secondary adrenal insufficiency?
Secondary adrenal insufficiency would be a hypo-secreting pituitary
Thus aldosterone would not be involved, so potassium would be normal
There would also be no hyperpigmentation
What is Waterhouse-Friderichsen syndrome?
Acute adrenocortical insufficiency due to adrenal hemorrhage
What are some things known to cause W.F. syndrome? 3
1. Neisseria meningiditis septicemia
2. DIC
3. Endotoxic shock
Pheochromocytoma: epidemiology
Most common adrenal medulla tumor in adults
Pheochromocytoma: from what is it derived
Chromaffin cells which are dervied from neural crest
Pheochromocytoma: what do they secrete and what does this cause
Dopamine, NE and Epi leads to eposodic hypertensive spells, with other related symptoms
Pheochromocytoma: how is it diagnosed
High urinary levels of HVA, VMA and metanephrine
Pheochromocytoma: association with other syndromes 3
1. NF1
2. MEN IIA
3. MEN IIB
Pheochromocytoma: treatment
With nonselective alpha blockers
1. Phenoxybenzamine: irrervible blocker used for pre-op control
2. Phentolamine: reversible blocker used for intra-op contral (more controllable)
Pheochromocytoma: what are the 5 P's 5
1. Pressure
2. Pain (headache)
3. Perspiration
4. Palpitations
5. Pallor
Pheochromocytoma: what is the rule of 10's
10 percent:
malignant
bilateral
extra-adrenal
calcify
affect kids
run in families
Pheochromocytoma: what is the metabolic pathway from phenylalanine to epinephrine and what are the detectable metabolic byproducts of each
Phenylalanine --> tyrosine --> L-dopa --> dopamine --> NE --> Epi
Dopamine converts to HVA (homovanillic acid)
NE converts to VMA (vanillylmandelic acid)
Epi converts to metanephrine
Neuroblastoma: epidemilogy
Most common adrenal medulla tumor in kids
Neuroblastoma: where can it also occur
Anywhere along the sympathetic chain
Neuroblastoma: what is a dx tool
Elevated urinary HVA or VMA
Neuroblastoma: comapare to pheo
Neuroblastomas don't cause HTN
Neuroblastoma: oncogene
N-myc
Hyper or hypothyroid: cold intolerance
hypo
Hyper or hypothyroid: chest pain
hyper
Hyper or hypothyroid: decreased appetite
hypo
Hyper or hypothyroid: weight loss
hyper
Hyper or hypothyroid: hyporeflexia
hypo
Hyper or hypothyroid: weight gain
hypo
Hyper or hypothyroid: hot and wet skin
hyper
Hyper or hypothyroid: palpitations
hyper
Hyper or hypothyroid: increased appetite
hyper
Hyper or hypothyroid: cool and dry skin
hypo
Hyper or hypothyroid: constipation
hypo
Hyper or hypothyroid: weakness
hypo
Hyper or hypothyroid: coarse, brittle hair
hypo
Hyper or hypothyroid: arrhythmias
hyper
Hyper or hypothyroid: hyperreflexia
hyper
Hyper or hypothyroid: lethargy
hypo
Hyper or hypothyroid: fine hair
hyper
Hyper or hypothyroid: diarrhea
hyper
Hyper or hypothyroid: facial and periorbital myxedema
hypo
Hyper or hypothyroid: hyperactivity
hyper
What is the best first screening for primary thyroid issues
TSH
What are the lab results for primary hypothyroidism 3
1. Increased TSH
2. Decreased total T4
3. Decreased free T4
What are the lab results for primary hyperthyroidism 3
1. Decreased TSH
2. Increased total T4
3. Increased free T4
What is the most common cuase of hypothyroid?
Hashimoto's thyroiditis
Hashimoto's: desribe the process
Autoimmune process where the thryoid follicles are slowly destroyed
Patient may be hyperthyroid early in the course (thyrotoxicosis)
Patient will eventually become hypothyroid
Hashimoto's: thyroid presentation
Thryoid will be moderatley enlarged and non-tender
Hashimoto's: histology 2
1. Lymphocytic infilatrate with germinal centers
2. Hurthle cells - enlarged epithelial cells that are eosinophilic and stain pink
Hashimoto's: what auto-antibodies 2
1. Anti-thyroglobulin
2. Anti-microsomal
Hashimoto's: Associated with what HLA type?
HLA-DR5
Cretinism: what is the problem
a syndrome due to severe fetal hypothyroidism
Cretinism: where does it tend to occur
anywhere where there is a lack of dietary iodine which leads to endemic goiter
Cretinism: in which country is it common still
China
Cretinism: what about sporadic cases 2
1. Due to defect in T4 production
2. Develepmental defect in thyroid gland formation
Cretinism: findings 6
1. Pot-belly
2. Pale
3. Puffy face
4. Protruding umbilicus
5. Protuberant tingue
6. Mental retardation
Cretinism: what does the word "cretin" mean
Christlike - those who were affect were thought to be so mentally retarded that they were incapable of sin
de Quervain's: what is another name
Subacute thyroiditis
de Quervain's: describe
May initially by hyperthryoid
Self-limited hypothyroidism often following a flu-like illness
de Quervain's: findings 3
1. High ESR (inflammation)
2. Jaw pain
3. Very tender thyroid
de Quervain's: histology
Granulomatous inflammation (multi-nucleated giant cells)
de Quervain's: difference between this and subacute/chronic lymphocytic thyroiditis
Hashimoto's is also called chronic lymphocytic and it is painless
Subacute lymphocytic is also painless and it tends to happen post-partum
de Quervain's is also subacute but very painful
What is Riedel's thyroiditis
This is a type of chronic hypothyroidism where the thyroid tissue is replaced with fibrous tissue.
How does Riedel's present
Fixed and rock-hard but painless goiter
Grave's: what type of disease
Autoimmune - type II hypersensitivity
Grave's: describe problem
Auto-antibodies which bind and stimulate TSH receptors leading to hyperthyroid
Grave's: findings 3
1. Proptosis and EOM swelling
2. Pretibial myxedema
3. Diffuse goiter
Grave's: when does it often present
During times of stress like childbirth
Grave's: what is a cause of death
Hyperthyroidism of any kind increases to density of beta-1 receptors on the heart
Therefore, a stress induced catecholamine surge is a potential cause of death in any hyperthyroid patient
Toxic multinodular goiter: describe problem
There are focal patches of hyperfunctioning follicular cells which are working independentally of TSH because they are mutated
Toxic multinodular goiter: are the nodules malignant
Even though this sounds cancerous - no they are not malignant
What is the Jod-Basedow phenomenon
A patient who has iodine deficiency goiter who is suddenly made iodine replete will become thyrotoxic
Thyroid cancer: which is the most common
Papillary carcinoma
Thyroid Papillary carcinoma: what is the prognosis
excellent
Thryoid Papillary carcinoma: histology 3
1. Ground glass nuclei (orphan annies)
2. Psammoma bodies
3. Nuclear grooves
Thryoid Papillary carcinoma: what increases the risk
Radiation in childhood
Thryoid Follicular carcinoma: what is the prognosis
good
Thryoid Follicular carcinoma: histology
Uniform follicles
Thryoid Medullary carcinoma: what is the origin
Parafollicular C cells
Thryoid Medullary carcinoma: what does it secrete
calcitonin
Thryoid Medullary carcinoma: histology
sheets of cells in amyloid stroma
Thryoid Medullary carcinoma: associations
MEN IIA and IIB
Thryoid Undifferentiated/anaplastic: prognosis
very poor
Thryoid Undifferentiated/anaplastic: occurs in whom
older folks
Thryoid Lymphoma: association
Hasimoto's thyroiditis
Hypercalcemia: what is the mnemonic
CHIMPANZEES
C = calcium ingestion (milk-alkali syndrome)
H = hyperPT or thryoid
I = iatrogenic
M = muliple myeloma
P = paget's disease
A = addison's disease
N = neoplasm
Z = zollinger ellison
E = Excess vitamin D
E = Excess vitamin A
S = sarcoidosis
Hypercalcemia: what is the common iatrogenic cause
thiazide diuretics
Hypercalcemia: what is the deal with Paget's disease
they usually have normal calcium but become hypercalcemic when immobalized
Primary hyperPT: what is a common cause
Usually a PTH secreting parathyroid adenoma
Primary hyperPT: what are the findings
Stones, bones and groans
1. Hypercalcemia
2. Hypercalciuria (stones)
2. Hypophosphatemia
3. Increased PTH
4. Increased alk phos (bones)
5. Increased urinary cAMP
6. Weakness and constipation (groans)
What is osteitis fibrosa cystica
The parathryoid glands are over active leading to painful cystic bone spaces that are filled with fibroous tissue.
What is osteitis fibrosa cystica also called
von Recklinghausen's diesase
This is not NF1 which is von recklinhausen syndrome
Secondary hyperPT: what is the cause
the PT glands become hyperplastic because there is decreased gut calcium absorption and increased phosphorus levels
Secondary hyperPT: where is it often seen
chronic kidney disease - so the whole process is secondary to decreased vitamin D
Secondary hyperPT: what are the findings 4
1. Hypocalcemia
2. Hyperphosphatemia
3. Increased alk phos
4. Increased PTH
What is renal osteodytrophy
Renal disease --> low vitamin D --> low calcium --> high PTH --> high bone turnover --> bone lesions
HypoPT: what are 3 common cuases 3
1. Accidental excision when doing a thyroid surgery
2. Autoimmune destruction
3. DiGeorge's syndrome
HypoPT: what are the findings
Hypocalcemia which is famous for causing tetany
HypoPT: what is Chvostek's sign
A sign that indiciates hypocalcemia:
tapping on the facial nerve ellicits facial muscle twitching
HypoPT: what is Trousseau's sign
A sign that indiciates hypocalcemia:
occlusion of brachial artery with BP cuff ellicits carpal spasms
What is pseudohypoPT
an autosomal dominant kidney condition where the kidney doesn't respond to PTH
What is another name for pseudohypoPT
Albright's hereditary osteodytrophy
What are the findings in pseudohypoPT 3
1. Hypocalcemia
2. Shortened 4th and 5th digits
3. Short-stature
Pituitary adenoma: what is it most commonly
prolactinoma
Prolactinoma: what are the findings 3
1. Bitemporal heminopsia due to compression of the optic chiasm
2. Amenorrhea - hypogonadism
3. Low libido - hypogonadism
Prolactinoma: what class of drugs is used to treat and give 2 examples
Dopamine agonist drugs cause tumor shrinkage: Bromocriptine and cabergoline
Acromegaly: what is the cause
Excess GH in adults
Acromegaly: what are the findings 5
1. Large tongue with deeps furrows
2. Deep voice
3. Large, doughy hands and feet
4. Coarse facies
5. Insulin resistance (GH increases glucose)
Acromegaly: what is it called in kids
Gigantism because excess GH accelerates linear bone growth
Acromegaly: what is the tx
Pituitary adenoma resection followed by octreotide administration (somatostatin analogue)
when is increased GH normal 3
1. Stress
2. Exercise
3. Hypoglycemia
Acromegaly: how to dx 2
1. Increased serum IGF-1
2. Serum GH does not fall after administering glucose load
Sheehan's: what is it
Postpartum hypopituitarism
Sheehan's: desribe process
During pregnancy, the anterior pituitary gets bigger due to lactotroph hyperplasia. However, the blood suppply does not change. At delivery, if there is severe bleeding the enlarged pituitary is now at increased risk of being infarcted
Sheehan's: findings 4
1. Fatigue
2. Anorexia
3. Poor lactation
4. Loss of pupic and axillary hair
DI: describe
Constant thrist and polyuria
Cannot concentrate urine due to malfunction in ADH pathway
DI: what are the 2 types 2
1. Central - lack of ADH production
2. Nephrogenic - ADH cannot bind to the kidneys
DI: what are some common cuases of central 4
1. Pituitary tumor
2. Trauma
3. Surgey
4. Histiocytosis X
DI: what are some common cuases of nephrogenic 3
1. Hypercalcemia - messes with tubular transport
2. Lithium - famous for this
3. Demeclocycline - a tetracycline abx that antagonizes ADH
DI: dx 3
1. Water deprivation test - urine osmolality does not increase (urine doesn't concentate)
2. Central DI: desmopressin adminstration causes urine to concetrate
3. Nephrogenic: desmopressin administration yields no change
DI: findings
Dilute urine with SG < 1.006
Serum is hypertonic > 290
DI: treatment for central
Intranasal desmopressin
DI: treatment for nephrogenic 3
1. Indomethacin
2. HCTZ
3. amilioride
DI: why give HCTZ for nephrogenic
It's complicated but the overall effect is to decrease:
1. Decrease water loss
2. Prevent hypokalemia
SIADH: desribe it
Anything whereby there is too much ADH acting in the body:
1. Excessive water retention - leads to hypotnic serum
2. Hyponatremia
3. Urine is more concentrated than the serum
SIADH: what is a problem with the sodium levels
Hyponatremia can lead to seizures
However, the levels must be corrected slowly because central pontine myelysis occurs if corrected too rapidly
SIADH: treatment 2
1. H20 restriction
2. Demeclocycline
SIADH: common causes 5
1. Ectopic ADH - small cell lung cancers
2. CNS disorder
3. Head trauma
4. Pulmonary disease
5. Drugs - cyclophosphamide
DM: what are the acute manifestations 6
1. Polydipsia - drink lots
2. Polyuria - pee lots
3. Polyphagia - eat lots
4. Weight loss
5. DKA in type I
6. Hyperosmolar coma
DM: what hormones are left unopposed when there is an insulin shortage? 4
1. Glucagon
2. GH
3. Epinephrine
4. Cortisol
DM: what is the eventual outcome of an untreated insulin deficiency
Dehydration and acidosis which lead to coma and death
DM: what are the 3 main ways that dehyrdration and acidosis occur in an acute insulin shortage
Insulin shortage (and unopposed other hormone excess) lead to:
1. Decreased glucose uptake
2. Increased protein breakdown
3. Increased lipolysis
DM: how does decreased glucose uptake in an insulin shortage lead to dehydration
Basically, hyperglycemia contributes to an osmotic diuresis where excess water is pulled into the tubules because there is so much solute
DM: how does increased protein breakdown in an insulin shortage lead to dehydration
Protein breakdow creates lots of free AA which are lost as nitrogen in the urine. This process also contributes to osmotic diuresis
DM: how does increased lipolysis in an insulin shortage lead to acidosis
Increased fat breakdown leads to increased free fatty acids in the blood. This triggers ketogenesis which is a starvation reponse. So ketone levels in the blood and urine are high. They also cause the blood pH to drop and so this is called DKA
DM: what are the 2 main ways that chronically high blood glucose causes damage? 2
1. Non-enzymatic glycosylation
2. Osmotic damage
DM: describe some manifestations of non-enzymatic glycosylation 5
1. Small vessel disease - the BM is diffusely thickened
2. Retinopathy
3. Glaucoma
4. Nephropathy
5. Large vessel artherosclerosis (and the following sequelae)
DM: describe some manifestations of osmotic damage 2
1. Neuropathy
2. Cataracts due to sorbital accumulation
Type 1 vs 2 DM: primary defect
Type 1: viral or immune destruction of beta cells
Type II: body becomes resistant to insulin
Type 1 vs 2 DM: insulin as part of tx
Type 1: always
Type II: sometimes
Type 1 vs 2 DM: age of onset
Type 1: < 30 (with exceptions)
Type II: > 40 (with exceptions)
Type 1 vs 2 DM: associated with obesity
Type 1: no
Type II: yes
Type 1 vs 2 DM: genetic predisposition
Type 1: weak
Type II: strong
Type 1 vs 2 DM: HLA association
Type 1: HLA-DR 3 and 4
Type II: no
Type 1 vs 2 DM: glucose intolerance
Type 1: severe
Type II: mild
Type 1 vs 2 DM: ketoacidosis
Type 1: common
Type II: rare
Type 1 vs 2 DM: beta cells
Type 1: decreased in number
Type II: amyloid is present
Type 1 vs 2 DM: serum insulin levels
Type 1: decreased
Type II: variable
Type 1 vs 2 DM: polyuria, polydipsia, thirst, etc (classic sx)
Type 1: yes
Type II: sometimes
DKA: in which type of DM is this seen
Type 1
DKA: what usually triggers it 2
1. Due to not taking insulin (non-compliance or non-treated)
2. Complaint patient has increased insulin demands due to a physiologic stress like infection
DKA: what is the process
Hyperglycemia without insulin ramps up lipolysis which then triggers ketogenesis from free FFA
This leads to ketone body formation (beta-hydroxybutyrate in greater concentrations then acetoacetate)
DKA: what are the exam findings 6
1. Kussmaul breathing (deep and rapid)
2. N&V
3. Abdominal pain
4. Psychosis
5. dehydration
6. Fruity smalling breath due to exhaled acetone
DKA: what are the labs 6
1. Hyperglycemia
2. High AG acidosis
3. Decreased bicarb
4. High blood ketones
5. High leukocytes
6. Hyperkalemia - due to K+ shift from inside cells which happens sue to low insulin
DKA: what are some complications 4
1. Mucormysosis
2. Rhizopus infections
3. Cerebral edema
4. Arrhythmias and heart failure
DKA: what is the treatment 4
1. Fluids
2. Insulin
3. Potassium
4. Glucose on standby if hypoglycemia ensues
DKA: why do you need to give postassium if DKA causes hypoerkalemia
Hyperkalemia from DKA is because lack of insulin causes K+ to shift out of cells into the serum
When insulin is given, the K+ gets sucked back into cells and hypokalemia ensues
Therefore, K+ must be co-administered to correct this treatment related hypokalemia
Carcinoid syndrome: how common
rare
Carcinoid syndrome: what are carcinoid tumors derived from
neuroendocrine cells
Carcinoid syndrome: what types of tumors are famous for this and what do they secrete
small bowel neuroendocrine tumors that metastasize to elsewhere
these tumors secrete 5-HT
Carcinoid syndrome: why doesn't this happen if these tumors don't metastasize
when they are confined to the small bowel, secreted seratonin is metabolized in the liver
Carcinoid syndrome: symptoms 4
1. Diarrhea
2. Flushing
3. Asthmatic wheezing
4. Right sided valvular disease
Carcinoid syndrome: of what organ is this the most common tumor
carcinoid tumors are the most common tumor of the appenidix
Carcinoid syndrome: dx
increased 5-HIAA in the urine
this is the metabolic product of serotonin
Carcinoid syndrome: what is the rule of 1/3s 3
1/3 of these tumors:
1. Metastasize
2. Present with a 2nd malignancy
3. are multiple
Carcinoid syndrome: tx
octreotide is a somatostatin analougue
Zollinger-Ellison: what is it
gastrin secreting tumor of the pancreas or duodenem
Zollinger-Ellison: what does it cause
recurrent ulcers
Zollinger-Ellison: with what syndrome is it associated
MEN I - this is one of the possible pancreatic tumors
MEN: what are the 3 types 3
1. MEN I
2. MEN IIA
3. MEN IIB
MEN: what is the eponym for MEN I
Wermer's
MEN: what is the eponym for MEN IIA
Sipple's
MEN: what is the eponym for MEN IIB
there is none
MEN: what is mode of inheritance?
All MEN syndromes are AD
MEN: what is the oncogene?
The ret gene is associated with MEN IIA and IIB
MEN: what is the mnemonic
3PUST 2PM 1PMMG
MEN I: desribe
3PUST
P = pituitary tumor
P = Parathyroid tumor
P = Pancreatic neuroendocrine tumors
U = ulcers
S = stones (from high PTH)
T = thyroid adenoma
MEN I: what do the pituitary tumors secrete
Prolactin or GH
MEN I: what does the parathyroid tumor secrete
PTH --> hypercalcemia --> kidney stones
MEN I: what are the possible pancreatic neuroendocrine tumors 4
1. Zollinger Ellison - secretes gastrin which causes ulcers
2. Insulinomas
3. VIPoma
4. Glucagonoma
MEN IIA: describe
2PM
P = pheochromocytoma
P = Parathyroid tumors (high PTH)
M = medullary thyroid carcinoma (secreting calcitonin)
MEN IIB: describe
1PMMG
P = pheochromocytoma
M = medullary thyroid carcinoma (secreting calcitonin)
M = marfinoid habitus
G = ganglioblastomas in the mouth and intestine