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258 Cards in this Set

  • Front
  • Back
How do anti histamines work?
Block action of histamine by blocking histamine receptors
Should the dosing of antihistamine be high or low?
High to keep effectiveness
Which generation of anti-histamine does a better job of not causing allergies
Second generation
Which generation of antibhistamines does not cause sedation?
second generation
Why do anti-histamines cause such bad side effects?
Becuase they not only fit into histamine receptor sites, they also fit into many other CNS receptors
Explain the contraindication of a MAO inhibitor with taking anti-histamine
MAO inhibitors act to leave more adrenergic transmitter in the synaptic cleft. Antihistamine is an anti-cholinergic. The signal amplification of the adrenergic along with the dulling of cholindergic balance will yield an adrenergic overdose
Why is it risky to give a patient with narrow-angle glaucoma an anti-histamine?
Antihistamine is an anticholinergic, which will cause pupil dilation, something you don't want with narrow angle glaucoma
Asthma and antihistamines together. Good idea?
No, Antihistamine causes increases of mucous secretion- somehting an asthmatic would not like
What are the side effects of first generation antihistamines?
Drowsiness- caused Primarily by first generation
GI: Dry mouth and eye, nausea, diarhea, and vommitting
What are the first generation anti-histamines, and what are there dosages?
All first generations are dosed every 6 hours:
List and explain the dosings of the second-generation anti-histamines?
Second Generations are given once a day- something that definitely helps compliance.
Name some advantages and disadvantages of second generation anti-histamines
1. Not centrally acting so they don't produce as many side effects.
2. They also increase patient compliance with qd dosing
3. Unfortunately, they become ineffective after a month, so you have to keep switching between them
How do mast cell stabilizers work?
Inhibit chloride channels in mast cell cell membrane
What type of patients will benefit from a mast cell stabilizer rather than a anti-histamine?
People with asthma and allergic reaction to antihistamines
How long does it take for mast cell stabilizers to work?
Weeks. Therefore, usually used in conjunction with anti-histamine or steroid(keeps inflammation down while mast cell stabilizers take hold)
What are the common mast cell stabilizers
Cromolyn sodium
What is the most commonly used non-narcotic analgesic?
How Do NSAIDS act centrally?
Have the ability to reset body thermostat in the hypothalamus= fever reduction
How do NSAIDS act peripherally
Pain relief via prostaglandin blocking
What if an NSAID blocks prostaglandins made by the COX-1?
GI problems ensue
What is the effects of NSAIDs on platelet aggregation?
Inhibit platelet aggregation via thromboxin A-2 blocking. Aspirin most well known. This will prolong bleeding
What is the contraindication for an asthmatic when taking NSAIDS
NSAIDS block prostaglandin synthesis, it thus shifts the eicosanoid metabolites in favor of leukotrienes which cause vasoconstriction.
What is the contraindication for Kidney disease?
Prostaglandins are integral for blood blow to the kidney. NSAIDS will decrease prostaglandin synthesis. This would be bad for a diabetic patient
What are the side-effects of NSAIDS?
CNS: HA, dizziness, insomnia, tinnitus (ASA)
GI: NV&D, anorexia, dyspepsia (digestive problems)
GU: Dysuria (pain with urination), nephritis, renal failure
What are the common NSAIDS?
Acetylsalicylic acid (Aspirin)
Ibuprofen (Motrin)
Indomethacin (Indocin)
Napoxen (Naprosyn)
Ketorolac (Toradol)
Celecoxib (Celebrex)- Selective COX-2
Valdecoxib (Bextra)
Do steroids favor or inhibit gluconeogensis?
Favor- bad for diabetics
What is the body's natural glucocorticoid which deals with stress?
How do steroids produce their anti-inflammatory effect?
Turn off selective mediators (cytokines, prostaglandins, and interleukins) which will decrease circulationg lymphcytes, macrophages, and neutrophils.
Where do the immune responding cells go in the presence of a steroid?
Lymph tissue
Consequently, taking a steroid will do what to your immune system?
Decrease the body's ability to fight infection
What components of the circulation do steroids increase?
Erythrocytes, Platelets, and Neutrophils
What kind of side effect do steroids have TSH production and natural nortisol production
Decreases (natural steroids like aldosterone and cortisol)
What effect do steroids have on Gastic acid production?
increase it
What effect does a steroids have on HPA (hypothalamus, adrenal cortex, pituitary) axis
Suppresses functions
Steroid effect on Blood pressure?
A steroid decreases tissue healing, why would you want this?
Slowing of a corneal ulcer would decrease scarring
What effect do steroids have on muscle tissue
wasting- something have trouble climbing steps
What percentage of people to steroids cause depression in?
If someone has liver problems, would you prescribe prednisone or prednisolone? Why?
Predisone is a prodrug which is converted to prednisolone in the liver. If a patient has decrease liver function, you would want to just give prednisolone
Which compound has an inflammatory index of 1?
What are the inflammatory indexes of :
What are the dosings for moderate, high, and massive. In which area do optometrists operate?
Moderate = 0.5 mg/2.2 lbs/d
High = 1 to 3 mg/2.2 lbs/d. 20-60 mg/day.
Massive = 15 to 30 mg/2.2 lbs/d

We operate in the low to high range. Anything more would must be co-managed
What is the false implication of "hypersensitivy?"
It is a readction to excessive amounts of Ag
In reality, what is a hypersensitivty reaction?
Disease resulting from immune mediated tissue damaging reactions
What is another name for type I immune injury?
Allergic and anaphylactic
Which antibody is responsible for Type hypersensitivity
What is the basic chain of events that cause Type I injury
Mast cells and basophils degranulate in response to two Fc portions of IgE binding and release histamine, arachadonic acid, platelet activating factor.
What is a late phase Type I reaction?
Arachadonic acid and platelet activating factor staying in the system, hurting the patient.
Why do we give patients allergy shots?
The hope of getting the body to produce IgG instead of IgE in response to antigen, thus disallowing Type I injuries
What is a another name for Type II immune injury?
What is the first mechanism of Type II
Ab causes complement activation resulting in lysis of cell death. This is what happens to a fetus in a mother.
What is the second mechanism for Type II
Abs recruit and activate inflammatory cells (macrophages). This results in complement chemotactic factors.
In Type II, what do macrophages do?
Go through "frustrated phagocytosis" where they cant phagocytose, so they throw up lysosomal enzymes. An example of this is Moorens ulcer in the Cornea and conjunctival epithelean tissues
What is the third mechanism for Type II immune injury. Give an example
Phagocytosis of complement or Ab-coated cells (opsonins). Hemolytic anemia where the patient producs Ab to RBC
What the fourth mechanism for Type II immune injury. Give an example
Ab- dependent cell-mediated cytotoxicity where Ab coats body tissue and Natural Killer cells destroy the tissue. Thyroiditis is an example of this
What is another name for Type III immune injury?
Immune comlex- mediated
What is the mechanism for for Type III immune injury
Unphagocytosed Ag-Ab complexes deposit in tissue, and active complement, forming anaphlotoxins C3A and C5a.
Where do type III injuries typicalls occur?
Blood vessals and kidneys. Recall that these vessals are very similar to eachother. Also happens in the joints
Women get type III much more often then men, give some examples of Type III injuries
1. Reactive arthritis (ReA)- Riders disease, can’t see, can’t pee, can bend a knee.
2. Systemic lupus erythematosus (SLE)- eye relation and neovascularization
3. Polyarteritis nodosa
4. Sjögren's syndrome- Destroys salivary and lacrimal glands.
What is another name for a Type IV injury?
Cell mediated (caused by T-Cells)
Who is the coolest person in the Class of 2012?
Jacob Eugene Hannon
Does Ab have any part in Type IV injury?
What are some examples of Type IV?
1. Poison Ivy and Poison Oak
2. Type 1 diabetes mellitus
3. Multiple sclerosis
4 Inflammatory bowel disease (Crohn’s disease)
5.Rheumatoid arthritis (RA)- Could be Type III depending upon responses
Since Type IV is T-cell mediated, is the response immediate, or does it take 2-3 days?
2-3 days
What are the two types of Type IV injury
1. Initiated by CD4+ T cells, Helper T-Cells (delayed-type hypersensitivity - DHT) Secrete cytokines to recruit macrophages
Tuberculin reaction is an example of this type of reaction. Tells whether or not someone has been exposed to tuberculosis.
2. Initiated by CD8+ T cells, Cytotoxic cells (direct cell cytotoxicity) Cytotoxic cells themselves are responsible for the damage. Found in Graft rejection
Why do some antigens provoke a type IV reaction and others provoke a type I?
No one knows
Explain what a type V injury is
Ab stimulate or block receptors
Give an example of Type V stimulating hypersensitivity
Grave's disease. Thyroid in constantly stimulates
Give an example of Type V blocking hypersensitivity reaction
Myasthenia Gravis
Type V is ofter class
Type II
What are some causes of Cell injury
Physical agents- heat or cold
Chemical agents and drugs
Infectious agents
Immunologic reactions
Genetic derangements
Nutritional imbalances
With severe or persistant stress, will the cell die?
Is cell injury reversible?
Up to a point yes
What is cell atrophy?
Shrink of cell by loss of substance. It is not death
What is atrophy caused by?
Age, Decreased blood supply, nutrition, and stimulation.
Are atrophied cells still viable?
Yes, they just require less energy to sustain
What is hypertrophy?
Increase structural synthesis without cells division
What are the different hypertrophy?
Hormonal (Transient): changes in breast during pregnancy
Compensatory: kidney enlargement when one is removed
Adaptive: muscle enlargement with exercise
What is hyperplasia?
An increase amount of cells
What are the two types of physiological hyperplasia
Hormonal: pregnancy
Compensatory: replacement of tissue
What are two types of Pathologic hyperplasia
Epithelial hyperplasia, usually from things like papilloma virus
What is Metaplasia
Cells switch type
What are two common forms of metaplasia
Epithelial metaplasia in smoking. Destroys columnar ciliated epithlium so body switches to stratified squamous. Body can’t clear mucous as well.
Mesenchymal Metaplasia: Fibroblasts to osteoblasts.
Can tissue return to normal after metaplasia?
What is dysplasia
Disorderly, non-neoplastic proliferation of cells
What are some hallmark of dysplasia
Architectural anarchy,
Trememendous cell and size variation
Which tissue do you normally see dysplasia in?
What is carcinoma In-Situ?
An advanced form of dysplasia over the entire thickness of tissue. Pre-neoplastic
What is neoplasia?
New, autonomous cell growth
What is the difference between benign neoplasms and malignant neoplasms?
1. Benign neoplasms- Usually floppy and moves around
Well-differentiated cells
Look and act like forbearers. I.E. if it was in the liver, the mass of growth looks like liver cells
2. Malignant neoplasms- does not move around when touched, attaches to underlying tissue. Anaplastic tissue present- doesn't look like it's forebearers. Could metsthesize
List things that can kill cells
Inability to reverse mitochondrial dysfunction
Cell membrane damage
Ca++ influx
Free radicals
What is necrosis
The sum of the degradative reaction occuring after cell death
What are the two types of Necrosis?
1. Autolysis
Self-digestion by cells own lysosomal enzymes
After death, all tissues autolyze
2. Heterolysis
Digestion by living white cells
What is the difference between a hormone and a cytokine?
Cytokines act more locally
What are some examples in which the endocrine systems is damaged by Immune injuries?
List the hormones which the pituitary release in the anterior lobe
ACTH, GH, Prolactin, LH, FSH, TSH, MSH
List the hormones which the pituitary secretes in the posterior lobe
Vasopressin, Oxytocin
How often is Prolactin (LH) secreted
All the time. Pitutary tumor will make it release even more
What does hyposecretion of LH result in?
galactorrhea (flow of milk from the breast) and amenorrhea (loss of menstruation) in women, and impotence and decreased libido in males
What does hypersecretion of LG result in?
headaches, infertility and weight gain in both sexes
ACTH influences the production of what?
Aldosterone, Adrogens, Glucocorticoids
What is hypersecretion of ACTH?
Hypersecretion results in “moon face”, “buffalo hump”, easy bruising (because they interfere with platelet aggregation from TX2 and prostaglanding pathway), acne (body can’t fight off infection), depression
What does hyposecretion do?
fluid loss with hypotension, hyponatremia( loss of salts), muscle weakness, and skin pigmentation changes (ACTH has a melanocyte stimulating hormone near the nipples)
What does Hypersecretion of TSH do?
Hypersecretion results in increased metabolic rate, tremor, heat intolerance, weight loss (diet pills have thyroid hormone). May also have tremor.
What does Hyposecretion of TSH do?
Hyposecretion results in decreased metabolic rate, cold intolerance, weight gain
What does FSH do?
Spermatogenesis in males, stimulates ovarian follicles to grow and produce estrogen in women
What does Luteinizing hormone do?
Stimulates testosterone synthesis in males, and estrogen and progesterone from the corpus luteum in women (maintain pregnancy in women)
Is Vasopression a vasoconstrictor or Dilator?
What does ADH do?
Promote Reabsorbtion at the level of the kidney
What type of Diabetes will insufficient ADH produce?
Diabetes insipidus
What will an excess of ADH do?
Hyponatermia (low Na level) and cerebral edema
Which hormone has a positive feedback loop?
What does oxytocin do?
Stimulates Uterine Contraction, milke ejection in lactacting women. Causes you to trust.
Does a pituitary adenoma usually cause increase or decreased levels of hormone release?
What percentage does it make up of symptomatic intracranial tumors
When do pitutiary tumors begins
Fourth the sixth decade
Are most pituitary adenomas benign or malignant?
Benign, but can still cause neurologic problems form physical intrusion
What is the cutoff measurement between macro-adenoma and microadenoma
1 cm
Which portion of the pituitary can a tumor afflict and what kind of secretion will it make
What are the most common disorders assocaited with pituitary adenoma?
1. Hyperprolactinemia(most common): amenorrhea, galactorrhea, impotence
2. ACTH: Cushing’s disease
3. Growth hormone: acromegaly
When do you usually see ocular involvement with pituitary adenoma?
When the tumor becomes a macroadenoma
How does a pituitary tumore usually affect the Cranial nerves?
Compression and movement into the cavernous sinus
What type of Visual field defect do you usually see with Pituitary tumors?
Bitemporal Hemianopsia. Usually beging in superior temporal field
What are some important features to diagnosis pituitary adenoma.
Headaches early in the morning.
Weight gain.
Loss of sexual drive.
What type of imaging is used to ID pituitary adenoma
CT and MRI with Gadolineum enhancement
What is the first step in therapy of Pituitary adenoma?
Pharacological intervention in the hopes resolution
What type of surgery is usually done with Pituitary adenoma
Transphenoidal surger
What percent of adenomas affect prolactin release?
fSometimes, there can be damage to the hypothalamus and pituitary stalk. What does this do in terms of Prolactin
Prevent decrease of hypothalamic dopamine, which is a check for prolactin levels. Thus, Loss of dopamine function will increase prolactin levels. Drugs could also interfere. MOI and cimetidine are examples
What types of medications will treat hyper prolactinemia
Dopamine agonists
WWhat are the two dopamine agaonists and their dosages for hyperprolactinemia?
1. Bromocriptine- Three times a day, orally or vaginally. Associated with tumor regression
2. Cabergoline- Twice weakly orally or vaginally.
What is issues in prescribing Dopamine agonists?
Bromocriptine is cheaper however has lower patient compliance because it must be taken twice to three times per day
Cabergoline is more expensive, however, it only has to be taken twice weekly
Describe Acromegaly
Excessive GH in adults- acromegaly
Results in growth in the soft tissues, bone
What are the clinical features of Acromegaly?
Enlargement of the jaw with separation of the teeth
Hand and feet enlargement
Entrapment neuropathies (carpal tunnel)
Abnormal glucose tolerance- Body needs energy. Brings on diabetes melitus. Makes tissues resistant to insulin as well
Heart failure (HF)
What movie is the greatest Movie of all Time?
Batman: the Dark Knight
What are the therapy interventions for Acrimegaly?
Transphenoidal surgery
Radiotherapy 3-10 normalization time
Pharmacological intervention
What two Somatostatin analoges that are prescribed for acromegaly? How often are they taken and what is the method of introduction
Both are Somatostatin Analogues
1. Ocreotide- given q8h SubQ. If effective, switch to injectable suspension q4w
2. Lanredotide- May be possible to give injection q6-8 wks
What Dopamine agonists are used treat Acromegaly?
Bromocriptine and Cabergoline. Could shrink tumor.
What are the growth hormone antagonists used to treat acromegaly
When are growth hormone antagonists used to treat acromegaly
When somatostatin and surgery does not work by themselves
What is another name for hypercorisolism?
Cushing's syndrome
What is the most common cause of Cushing's syndrome?
Exogenous introduction of steroids. usually not created with topical steroids
Explain the difference between Cushings Disease and syndrome
Cushings syndrome is ALWAYS elevated levels of steroid in the body. Cushings disease is whenever that elevated level of steroid is from a pituitary tumor
How many cases of raised steroid levels are cushing's disease?
How many times more frequent do women get Cushings than men?
5 times
When do you get Cushing's disease
Third to fourth decade
Would a hypersecreting tumor in the Adrenal gland be considered Cushing's disease or Cushing's syndrome?
Is a hypersecreting tumor or hyperplasia in the adrenal gland ACTH dependent or independent?
What percent of cushings syndrome is accounted for with a hypersecreting tumor or hyperplasia in the adrenal gland?
Is it more common to have hyperplasia or neoplasm in the adrenal gland?
What is ectopic ACTH secretion?
A neoplasm, usually in the lung, that secretes ACTH.
Is an ectopic ACTH secreting tumor responsive to input from the hypothalamus?
What percentage of Cushing syndrome does an ectopic ACTH secreting tumor account for?
What are the clinical Symptoms and characteristics of Cushing's syndrome
Gradual weight gain

Later: Truncal obesity
Moon face
Buffalo hump
Muscle weakness (can't climb stairs)
Hyperglycemia- 20% of patients have Diabtets
Thinning of skin
Increased infection
Hirutism- Body hair
What test is used to differentially diagnose Cushing's disease? Describe it
Dexamethasone suppression test. Most of the time, the tumor in the pituitary will still respond a little to the hypothalamus. If you give a massive steroid, the hypothalamus will put the breaks on ACTH. This will lower endogenous steroid. It the tumor is elsewhere (lung) endogenous steroid levels will not increase
What is the preferred treatment for cushings disease
Transphenoidal surgery
What is adrenalectomy?
Removal of the adrenal gland, leaves patient with Addison's disease.
Other than addison's, what would be a side-effect of adrenal-ectomy
Rapid tumor growth (nelson's syndrome)
Does adrenal carcinoma prognosis good?
What is the primary aldosterone syndrome known as Conn's syndrome
Aldosterone secreting adenoma of the adrenal gland. 60-80% of primary hyperaldosteronism cases are this.
What is the etiology behind Conn's syndrome?
Hypertension due to increase sodium and hypokalemia to to potassium insufficiency.
What are the symptoms of Conn's syndrome?
Tetany- inability to contract muscles
Parasthesia- Inability for muscles to contract
At what proportion does conn's syndrome affect the population?
Women/men in a ration of 2/1
What causes secondary hyperaldosteronism?
Anything other than a tumor. Usually poor output. Body then ramps up Renin-angiotensins system to compensate.
What are the causes of acute adrenal insufficiency?
1. Patient with chronic insufficiency having a massively stressful event
2. Sudden witdrawal from exogenous steroids after patient's adrenal has atrophied- patients should be taper off to reduce this possibility
What is chronic Adrenal insufficiency?
Progressive destruction of the adrenal cortex
What are the causes
Autoimmune, Tuberculosis, and metastic neoplasms
What are the clinical features of Chronic adrenal insufficienty
1. GI disturbances
2. Hypotension (secondary to loss of aldosterone)
3. hyperpigmentation- Too much melanocyte stimulating hormone
4. Weakness
HyWhat is the difference between the Adrenal medulla and adrenal cortex
Medulla is the neurologic tissue that is at the center of the adrenal cortex
What type of cells make up the adrenal medulla?
Chromaffin cells- secrete and synthesize epinephrine
TWhat is pheochromocytoma
Tumor of the adrenal medulla which gives rise to massive sympathetic discharge- symptoms include everything you would think of with such a burst
Why is it called the 10% tumor?
10% malignant
10% bilateral
10% tisue outside adrenal
10% in Children
10% runs familialy
10% recur
10% present with stroke
What is increased cardiovascular risk with Pheocrhomocytoma?
Stroke from myocardial ischemia (heart beats so fast it can't supply itself with blood). Leads to renal failure in kidney
What is the most commonly disdiagnosed disease
Thyroid Eye disease
Follicles in thyroid are filled with what?
Thyroglobulin- precursor to thyroid hormone
What are the percentages of production of T3 and T4. Discuss which one is more effective
Body makes 20 times more T4, however T3 is 5 times more biologically active
How is most thryoid found in the blood
Bound to Thyroid binding globulin (TBG). It stays this way till the body needs it
When unbound, what does thyroid hormone do?
Up-regulates carbohydrate metabolism, lipid metabolism, and increases protein synthesis which results in a net increase of the metabolic rate
When can you get Goiter?
Any time! You are most likely to get it during a hypothyroid state from the glands attempt to become hyperplasic or hypertrophic to compensate for lack of hormone. You can get goiter during Euthyroid and hyperthyroid state.
Increased T3 and T4 cause what disease?
What are the common causes of thyroid toxicosis?
1. Graves- Most common
2. Ingestion of too much thyroid
3. Hyperfunctional multinodular goider
4. pituitary adenoma very rare (you can get thyroid tumor, but it usually causes nothin)
What are some clinical features of Thyrotoxicosis
1. INcreased metabolism
2. Nervousness, irritability
3. Tachycardia- Most common symptom
4. Hypermotility of gut- leads to dehydration
5. Staring + lid retraction
6. Heat intolerance
7. Insomnia
8. Scanty menstrual periods
What percentage of the population has grave's
When is Grave's peak incidence?
20-40 years
At At what incidence will women get graves as compared to men?
What SNP is associated with Grave's disease?
What are the levels of TSH in the blood during Graves disease?
Very low, because the the hypothalamus does not want any more thyroid even though there is a massive amount in circulation
What is the triad of Grave's disease?
2. Opthalmopathy In 40-50% Exopthalmos from swelling of EOM (patient could be seeing double). Lid retraction, edema, keratitis and compressive optic neuropathy
3. Pretibial Myxedema- Thickening of tissue under the skin in the lower legs
What is the Beta-Block that is used to treat Grave's
How do antithyroid drugs work?
Inhibit the oxidation of iodine and thus decrease thyroid hormone synthesis
What are the two antithyroid drugs?
1. Propyhthiouracil- one pill everyday. Acts faster and is one third the price of methimazole
2. Methimazole- same dosage of propylthiouracil.
How are antithyroid drugs scheduled?
Continue for 1-1.5 years with tapered does in hopes that patient becomes Euthyroid (aka stop producing thyroid stimulating immunoglobuline)
What are some problems with thyroid paramacological innerventions
1. Remission less than 20%
2. Side effects- Rash and joint pain, Agranulocytosis (don't produce Granulocytes- EVER AGAIN)
What are the advantages to thyroidectomy?
Rapid cure and low rate of becoming hypothyroid
What are some risks of thyroid surgery
Damage to parthyroid gland and damage Laryngeal nerve (you can't talk!)
What type of iodine is used in radioactive iodine therapy
iodine 131
What does Radio iodine function do?
Reduces thyroid size and function within 6-12 weeks
What are some advantages to radioactive iodine treament
Cure rate approaches 100%, but most likely patient will become hypothyroid. 70% have become hypothyroid after 10-15 years
What is the difference between primary hypothyroidism and secondary hypothyroidism
Primary hypothyroidism means that the thyroid isn't producing sufficient amounts of hormone. High TSH, low thyroid
Secondary- Thyroid works find, just not being stimulated by the pituitary and hypothalamus
What are the causes of hypothyroid
1. Removal of thyroid or radioactive therapy
2. Hashimoto's disease
3. Primary idopathic hypothyroidism- 5% of population has this affliction
What are the clinical features of hypothyroid
Just the opposite of hyperthyroid
Generalized apathy and mental sluggishness
May mimic depression early in disease
Slow speech
Cold intolerance
Delayed DTR
Decreased bowel motility with resultant constipation
Bradycardia, heart failure
What is cretinism?
Hypothyroid in children due to lack of iodine in diet or inborn metabolic error. Short stature and CNS impairment. Could occur in Utero
When is Jake Hannon's Birthday?
June 13, 1984
What is Hashimoto's disease?
Immune destruction of TSH receptors on the thyroid gland
What SNP is associated with Hashimoto's disease?
What is prevalence of Hashimoto's disease in women?
What is Hashitoxicosis
Transient hyperthyroidism that is followed up by the profound hypothyroidism that is hashimoto's disease
What is Hashimotos treated with?
L-Thyroxine qd. May be possible for weekly adminitstration
In the thyroid, even though it shouldn't be used to diagnose cancer, how can you determine between a benign and malignant tumor of the thyroid
Nodules that take up radioactive iodine are benign
Nodules in younger patients are more likely to be neoplastic
Nodules in males are more likely to be neoplastic
What is the treatmnt of parathyroid disfunction
Surgical removal
What are the two signs of Hypoparathyroidism
- Chvostek’s sign: Tap on facial nerve in front of ear causes contraction of facial muscles and upper lip
-Trousseau’s sign: Inflation of BP cuff for 3 minutes causes carpal spasm (MCP flexion with PIP (proximal interphalangeal) and DIP (distal interphalangeal) extension and adduction of thumb). Cerebral Palsy like thing in the hand.
What is syndrome X?
Insuline resistance syndrome
What are the increased risk of syndrome X for DM and cerebrovascular disease?
3X Cerebrovascular
What are the characteristics of some one with DM?
Central body weight obesity
Insuling resistance
Lipid abnormalities- Lipid abnormalities
Triglycerides > 150mg/dL
Low HDL: M < 40 mg/dL, and W < 50 mg/dL
Elevated BP- >130/85 mmHg
hWhat percentage of the population is Type 1 diabetic
What is prevalence of Type I Diabetes
160/100000. Mostly children
What are the histocompatability complexes associated with Type I diabetes
HLA-DR: 3 or 4 for Caucasians, 7 for African descent, 9 for Japanese)
What is the subroup 1 of Type I diabetes
LADA- Latent autoimmune Diabetes in Adults. Usually adults over the age of 35
What is LADA
Slowly progressive form of type I DM
A positive result for which compound will diagnose LADA
Glutamaic acid Decarboxylase
What type of medications to LADA patients become resistant to?
What is the prevalence of Type II diabetes
Prevalence is ≈ 6,670 per 100,000 population
What are the inflammatory markers seen prior to devlopment of Type II diabetes?
IL-6 and CRP
Whater percentage of type II diabetic are obese?
When diabetic, a patients live is secreting free glucose into the blood stream even though there is plenty there. Why?
Because the body can't take glucose into the cells, so it thinks that it is starving. So it releases glucose from the liver.
What are the factors which could contribute to Type II diabetes?
1. Decreased uptake of glucose
2. Decreased receptors on cells
3. decreased activity of peroxisome proliferator-activated receptors (PPAR) that controls the entry of sugar and fat into cell’s nucleus.
4. Excessive protein production in the PTPN1 gene
5. Deficiency in osteocalcin
What is diabetes 1.5
More of a blending of the type diabetes. They are an obese patient presents with positive antibodies against their Beta cells. Sometimes referred to as LADA which is incorrect. LADA are thin
What is the condition of being diagnosed with Maturity onset diabetes of the young *MODY)
Must have a family member who developped it before the age of 30
How many genes have been implicated with Maturity onset diabetes of the young (MODY). How many variants
Single gene.
6 variants
How is MODY controlled?
Low dose insulin, diet, or oral drugs
Is gestational diabets a form of type I or Type II
Type II
When doe gestational diabetes remit?
after delivery
Most Gestational diabetics will require what?
Does gestational diabetes increase the risk of type II diabetes later in life?
What are the symptoms of Diabetes mellitus
1. Polyuria
2. Polydipsia
3. Fatigue
4. Possible weight loss
5. Infections from decreased WBC activity and great media for bacteria in the blood
At about what concentration of blood glucose will the glucose spill over into the urine
In Diabetes, what does the liver make from free fatty acids to serve as an energy source
Ketones will result in what three symptoms
Ketonemia, ketouria, and ketoacidosis (pH of blood drops beneath 7.2)
What level of plasma glucose is considered diabetic no matter what time of day?
greater than 200 mg/dl
What level of fasting plasma glucose is considered diabetic
Greater than 126 mg/dl
What accounts for the fact that blood glucose is always 15% lower than plasma glucose?
Portions of blood glucose are bound to hemoglobin, making the amount of testable glucose in the blood 15% of plasma
True of false. Diabetes affects only tissue that is glucose reliant
False. Many times it is the tissues that don't need glucose that are damaged
What are the percentages of Type I and Type II diabetics that develop Renal failure?
Type I 30-50% (Major cause of death)
Type II 6-9%
What drug will protect kidneys during diabetes
ACE inhibitors
What is the first clinical sign of nephropathy in diabetics
Microalbuninuria (trace amounts of alubin in the urine)
A good rule of thumb, if you are damaging the kidney, what are you also most likely damaging
blood vessals
What is the leading cause of death is Type II diabetics
Heart disease
A diabetic's chance of getting a myocardial infarction is the same as who's
Some one who has already had a myocardial infarction
Diabetics experiencing peripheral vascular disease will ahve what symptoms
1. Claudication (limping)
2. Skin ulcers from poor circulation
3. Gangrene
Diabetes causes what percentage of non-traumatic amputations?
Diabetics experience peripheral vascular disease how much more often than normal people
4 Times
What are signs linked to PVD?
A. Leg pain relieved by rest
B. Cold feet with reduced or absent pulses
C. Nocturnal leg pain relieved by dangling legs over side of bed or walking
D. Loss of hair on the foot and toes
What percentage of DM patients experience neuropathy
What portion of the neurons are usually destroyed in Diabetic Neuropathy
Schwanns cells
What are some signs of neuropathy in DM
1. Paresthesias (pins and needles)
2. Decreased vibration sense
3. Decreased DTR (deep tendon reflex)
4. Slower conduction velocity
Neuropathy linked with peripher vascular disease is pernicious to diabetics because?
They can't feel ulcers growing on the bottom of their feet
What are some ocular signs and symptoms of DM
1. Flucuation in vision
2. Retinopathy caused by new, leaky blood vessals
3. Glaucoma
4. Heart failure signs from fundus exam
5. Cataracts
What is a Glycosylated end Product? What is it a function of?
non-enzymatic binding of glucose to proteins in body tissue. It is a function of how much plasma glucose you have. more glucose, more glycosylated end products