Mix8 Flashcards

1
Q

Broad casts are seen in what type of renal disease?

A

Chronic Renal Failure. Arise in dilated tubules of enlarged nephrons that have undergone compensatory hypertrophy in response to reduced renal mass.

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2
Q

Fatty casts are seen in what type of renal disease?

A

Nephrotic syndrome

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3
Q

What is the mechanism of muscle atrophy in Cushing’s Disease?

A

Cushing Disease = hypercortisolism. Myopathy in Cushing’s generally presents as proximal muscle weakness and is due to catabolic effects of cortisol on skeletal muscle&raquo_space; muscle atrophy.

** Glucocorticoid induced muscle atrophy is due to inhibition of Akt-1 (intracellular signaling molecule w/tyrosine kinase function). Can also be due to interference with insulin like growth factor 1. Finally, glucocorticoids can decrease muscle cell differentiation and protein synthesis.

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4
Q

Why do you have lid proptosis in Grave’s disease?

A

Graves = TSH R auto-Ab stimulate thyroid hormone production&raquo_space; hyperthyroidism&raquo_space; ^ sensitivity to catecholamines and ^ sympathetic activation&raquo_space; contraction of superior tarsal muscle.

** BUT true exophthalmos is only seen in Graves because you have T cell activation/stimulation of orbital fibroblasts and adipocytes by TSH-R Ab&raquo_space; orbital tissue expansion.

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5
Q

If an older women presents with headache, jaw claudication, muscle fatigue and visual disturbance with scalp tenderness what would be the most likely Dx? What sequellae would you have to look out for?

A

Dx = giant cell arteritis

Most common complication of GCA is aortic aneurysm dilation because the giant cell arteritis can involve branches of the aorta.

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6
Q

What are the 4 predominant ECG findings of Hyperkalemia?

A
  1. Tall peaked T wave.
  2. Short QT interval
  3. PR interval prolongation + QRS widening
  4. Disappearance of P wave

Can have conduction blocks, ectopic beats, or sine wave patterns.

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7
Q

What initial treatment is needed for treatment of hyperkalemia with evidence of ECG changes?

A

Calcium gluconate to stabilize cardiac myocyte membrane causing it to be resistant to effects of hyper K.

Need to give IV (not SQ) insulin + glucose + beta agonist (albuterol) to shift K+ back into the cells. Follow up with diuretics, exchange resins (sodium polysterine/kayexalate), and hemodialysis.

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8
Q

What is the cell type of origin of medullary thyroid cancer?

A

Medullary thyroid cancer is due to a calcitonin producing tumor arising from neuroendocrine parafollicular C cells of the thyroid gland.

** Could be a component of multiple endocrine neoplasia (MEN 2a/2b) so you should check for fractionated metanephrine assay to rule out life threatening hypertensive crisis from pheochromocytoma.

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9
Q

What is the low dose dexa suppression test used to evaluate?

A

Cushing Disease

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10
Q

What’s the first line treatment for acute glaucoma?

A

Mannitol administered IV, works immediately. Acetazolamide (CA i) can be used to prevent further production of aqueous humor&raquo_space; decreased intraocular pressure. Pilocarpine can be used to open canals of schlemm and provide immediate drainage.

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11
Q

Inflammatory acne is typically treated with benzoyl peroxide and topical retinoids. If Rx is refractory, would you add topical or PO abx?

A

Topical first (erythromycin, clindamycin). Then use PO Abx (tetracyclines) for refractory cases, or in cases where the area of skin covered is too large to use topical Rx.

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12
Q

What’s the typical age presentation for Sjogren’s syndrome?

A

Typically middle age (later presentation is unusual). Can occur independently or as a manifestation of another autoimmune disorder (i.e. systemic sclerosis).

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13
Q

What is a potential complication of actinic keratosis?

A

Progression to squamous cell carcinoma.

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14
Q

How would serum iron, TIBC, and ferritin levels present in iron deficiency anemia?

A

In iron deficiency anemia, serum Fe is low, TIBC is ^, and serum ferritin is decreased.

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15
Q

What are the two phases of metabolic alkalosis?

A
  1. Generation phase - Vomiting&raquo_space; depletion of total body acid as well as fluid, sodium, and chloride. Typically, acidic gastric secretions stimulate the pancreas and liver to excrete bicarb into the duodenum. But this doesn’t happen with repeated vomiting, so bicarb builds up&raquo_space; metabolic alkalosis.
  2. Maintenance phase - RAAS system retains water at the expense of losing K+ and acid in the urine despite total body acid depletion.

** Restore extravascular volume with IV NS to remove the stimulation of RAAS and enhance kidneys ability to excrete excess bicarb.

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16
Q

What’s the primary treatment of variceal hemorrhage in patients with cirrhosis?

A

Propanalol

17
Q

What is the MOA of tetanus toxin?

A

Bacteria enters skin through break, binds peripheral nerve terminals, goes to neuromuscular junction via retrograde axonal transport and ends up blocking RELEASE of inhibitory NT glycine and GABA&raquo_space; motor neuron disinhibition&raquo_space; ^ muscle tone + spasm

** Botulism impairs presynaptic ACh release and presents with symmetric descending flaccid paralysis, blurred vision, and areflexia. May cause diaphragmatic paralysis.

18
Q

What therapy should be offered to patients with A-fib and rapid ventricular response?

A

Rate control should be attempted with CCB (diltiazem) or B blocker. If hemodynamically unstable then use immediate cardioversion.

19
Q

What tool is used to evaluate risk of thromboembolic formation in A-fib?

A

Regardless of whether rate or rhythm control is used to treat A-fib, use CHADs VASC score to evaluate risk of thrombosis:

C- CHF 
H - HTN 
A2 - Age > 75 
D - DM 
S2 - Stroke/TIA/Thromboembolism
V - Vasc disease (prior MI, peripheral artery Dz, aortic plaque) 
A - Age 65-64
Sc - Sex (female)
20
Q

Ecythema gangrenosum is most often due to what bacterial infection?

A

Typically due to Pseudomonas infection (esp in the case of profound neutropenia)

21
Q

If a young man (24) presents with HTN, and the following ECG changes (normal sinus rhythm, high voltage QRS complex, downsloping ST depression, and T wave inversion in V5/V6, then what should be the next step in evaluation of the patient?

A

This is evidence of LVH in a young patient. Bilateral arm and leg measurements should be done to check for coarctation of aorta as a secondary cause of HTN because this guy is too young for CAD.

22
Q

What treatment should you offer to a patient with cyanide toxicity?

A

Hydroxocobalamin or sodium thiosulfate. Both bind directly to KCN molecules. Can also induce methemeglobinemia in with nitrites to increase ferric iron (Fe3+) in circulating Hb. Cyanide binds Fe3+ so methemeglobin provides an alternative site.

** Remember that cyanide inhibits cytochrome oxidase in ETC. Prevents aerobic respiration so cells switch to anaerobic metabolism&raquo_space; lactic acid formation and metabolic acidosis.

23
Q

If traveling to an endemic area for malaria, what prophylactic measures need to be taken?

A

Chemoprophylaxis with atovaquone-proguanil, doxy, or mefloquine. Mefloquine should be given 2 weeks before departure, during the time there, and 4 weeks after returning home.

24
Q

What treatment options should you offer a patient with a case of subacute thyroiditis?

A

Treatment is symptomatic with B-blockers for ctrl of thyrotoxic symptoms and NSAIDs for pain relief. Glucocorticoids can be used for severe thyroid pain not responding to NSAIDs.

Thyrotoxic phase is generally self limited.

25
Q

Why may you develop hearing loss with HIV treatment?

A

Serous otitis media is the most common ear pathology assoc with acquired immunodeficiency and is due to auditory tube dysfunction from HIV lymphadenopathy or obstructing lymphomas. Shows up as middle ear effusion without evidence of acute infection.

Conductive hearing loss with dull tympanic membrane.