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MS3 > Internal Med 11 > Flashcards

Internal Med 11 Flashcards

1
Q

Tx of urethritis

A
  • Almost always STD (Gon/Chla)
  • Tx = CTX + Azithro or Doxy
  • HIV screen
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2
Q

Tx of asymptomatic bacteruria

A
  • Only treat if pregnant or with urinary procedure

* Tx in pregnancy = Amoxicillin

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3
Q

Tx of uncomplicated cystitis

A

o Empiric: TMP/SMX, Nitrofurantoin, Fosfomycin

o 3 days

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4
Q

Tx of complicated cystitis

A

o Empiric: TMP/SMX, Nitrofurantoin, Fosfomycin

o 7 days

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5
Q

Tx of pyelonephritis

A

o IV = CTX
o PO = Cipro
o 10 days

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6
Q

Tx of perinephric abscess

A

o I&D
o Abx same as pyelo but for longer
♣ CTX
o 14 days

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7
Q

What are the major criteria of Endocarditis

A
  • Bacteremia
  • New regurg murmur
  • Vegetations on echo
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8
Q

What are the minor criteria of endocarditis

A
  • Risk factors (IV drug use, h/o endocarditis, prosthetic valve)
  • Fever >38
  • Vascular complications (splinter hemorrhages, janeway lesions)
  • Rheumatologic complications (Osler nodes, glomerulonephritis)
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9
Q

Tx of endocarditis

A

Abx for 4-6 weeks

♣ Native valve
• Vancomycin

♣ New prosthetic valve (<60 days)
• Vanc + Gent + Cefepime

♣ Old prosthetic valve (>365 days)
• Vanc + Gent + Ceftriaxone

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10
Q

When do you get surgery for endocarditis

A
  • Pt has developed CHF
  • Vegatation >15 mm
  • Vegetation >10 mm with embolism
  • Abscess (abx won’t work)
  • Fungus
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11
Q

What does Hyperkalemia do to EKG

A
  • Peaked T-waves

* Then everything gets stretched out (PR interval prolonged, widened QRS, torsades)

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12
Q

What does hypokalemia do to EKG

A

Prolonged QT, flattened T-waves, U-waves

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13
Q

What does hypocalcemia do to EKG

A

On EKG: prolonged QTc

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14
Q

What does hypercalcemia do to EKG

A

On EKG: shortened QTc

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15
Q

What is Zosyn

A

Pip/Tazo

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16
Q

What is Unasyn

A

Amp/Sul

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17
Q

What is Augmentin

A

Amox/Clav

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18
Q

Is the TSH likely to be high or low in thyroid cancer

A

High - thyroid cancers are usually NOT hyperfunctioning (no hyperthyroidism in cancer)

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19
Q

What will you see in papillary thyroid carcinoma

A

• Histology:
o Orphan Annie eye nuclei
o Nuclear grooves
o Psammoma bodies

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20
Q

What will you see in follicular thyroid carcinoma

A

• Histologically the same as follicular adenoma but invade the tumor capsule
o This finding is made on exam of a surgically excised nodule
Cannot differentiate based on histology
- Metastasis is usually hematogenous (vs. most which spread via lymph)

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21
Q

What will you see in medullary thyroid carcinoma

A
  • From parafollicular “C cells”
  • Will have increased calcitonin (hypocalcemia)
  • Associated with MEN 2A and 2B
  • Does not respond to radioactive iodine (C cells are not making iodine)
22
Q

How might diabetes affect the GI tract

A

Diabetic autonomic neuropathy of the GI tract (e.g. delayed gastric emptying)

23
Q

How do you treat diabetic gastroparesis

A

Metoclopramide (D2 receptor antagonist) has prokinetic and antiemetic effects

24
Q

What will you see in the fluid of a loculated pleural fluid collection caused by pneumonia

  • Glucose
  • pH
  • protien
A

Will be an exudative effusion

  • Low glucose (<60) due to consumption by bacteria
  • low pH (<7.2) due to anaerobic utilization of glucose by neutrophils and bacteria
  • High protein due to increased microvascular permeability due to cellular destruction
25
Q

What is the most effective non-pharmacologic measure to decrease BP

A

Weight loss

26
Q

What is the first step in someone with Cushing’s syndrome

A

Cushing syndrome = increased cortisol

First step is to measure ACTH

27
Q

What does Cushing syndrome + low ACTH mean

A

Adrenal tumor or exogenous glucocorticoids

28
Q

What is the next step if Cushing syndrome + high ACTH

A

Now you suspect Cushing disease (ACTH-pituitary adenoma) or ectopic ACTH secreting tumor

Need to do a high dose Dexamethasone suppression test

29
Q

Describe results of high dose dexamethasone suppression test

A

♣ Cortisol levels will decrease if Cushing Disease (ACTH-pituitary adenoma)
♣ Cortisol levels will remain elevated if ectopic tumor

30
Q

What is Addison disease

A

♣ Primary adrenal insufficiency problem of the adrenal gland
• Most commonly due to autoimmune destruction of adrenal gland

31
Q

Presentation of Addison disease

A

o Lack of cortisol = Weakness, fatigue, weight loss, abd pain, N/V, hypoglycemia
o Lack of aldosterone = hypotension, hyponatremia, hyperkalemia
o Increased ACTH = skin hyperpigmentation (due to POMC)

32
Q

Describe presentation of Secondary adrenal insufficiency

A

♣ Secondary adrenal insufficiency = problem of anterior pituitary
• Presentation:
o Lack of cortisol due to decreased ACTH weakness, fatigue, weight loss
o Aldosterone synthesis is preserved (controlled by RAAS) no hypotension or hyperkalemia
o ACTH low no hyperpigmentation

33
Q

What is Conn Syndrome

A

♣ Primary hyperaldosteronism:
• Aka Conn syndrome
• Due to adrenal adenoma
• Will see decreased renin due to negative feedback

34
Q

Describe presentation of Hyperaldosteronism

A

• Hypertension
• Hypokalemia
• Metabolic alkalosis
o Aldosterone causes increased H+ urinary loss
o Decreased K+ causes cells to push out K+ in exchange for taking up H+

35
Q

How do you distinguish Primary hyperaldosteronism from secondary hyperaldosteronism

A

Primary = will have decreased renin due to neg feedback

Secondary = high renin (this is the primary problem)

36
Q

Causes of secondary hyperaldosteronism

A

o Renal artery stenosis
o Congestive heart failure
o Low protein states (decreased osmotic pressure leads to low blood volume)

37
Q

Tx of pheochromocytoma

A

o Surgical resection, but first give:
♣ Alpha-blockers (Phenoxybenzamine)
♣ Can also add on beta-blockers
• Do not give beta-blockers first – will lead to unopposed alpha vasoconstriction and hypertensive crisis

38
Q

Describe pathogenesis of DKA

A

• Lack of insulin means glucose cannot get into the cell for glycolysis to make ATP = cell instead uses fatty acid beta oxidation which breaks down into ketone bodies

39
Q

Will sodium be high or low in DKA

A

o Hyponatremia due to sodium loss via diuresis (osmotic diuresis due to increased glucose)

40
Q

Will potassium be high or low in DKA

A

• High serum potassium but low total body potassium
o Cells will exchange H+ for K+ causing high potassium
o Potassium in the blood will be excreted causing low total body potassium

41
Q

Tx of DKA

A

• Insulin to treat hyperglycemia
• Give potassium BEFORE insulin
• Fluids – pt will be dehydrated due to osmotic diuresis
• BMP to check for anion gap
o Stop ICU level management once gap closes
o If glucose normalizes but gap is still open, you need to continue fluids but can switch to D51/2

42
Q

What is the major complication of Type 2 DM

A

o Hyperosmolar hyperglycemic nonketotic syndrome (HHS)
♣ Hyperglycemia -> excessive osmotic diuresis -> dehydration -> HHNS
♣ Symptoms: thirst, polyuria, lethargy, focal neurological deficits (e.g. seizures), can progress to coma and death

43
Q

What will you see in blood sugar, ketones, and pH in HHNS

A

♣ Labs: hyperglycemia (800-100), dehydration, increased serum osmolarity, no acidosis
• Ketone production inhibited by presence of insulin (T2DM still have some insulin production)
• Blood glucose will be a lot higher than in DKA because pt isn’t as sick, so sugar has more time to go up before pt presents

44
Q

What are the infectious causes of esophagitis

A
  • Candida
  • HSV
  • CMV
  • HIV
45
Q

Tx of eosoniphilic esophagits

A
  • PPI

- If PPI does not fix problem, then give aerosolized steroids

46
Q

What are the symptoms of scleroderma

A

♣ CREST syndrome:
• Calcinosis (calcium deposition) / anti-centromere antibody
• Raynoud
• Esophageal dysmotility
• Sclerodactyly (tightening of skin with loss of wrinkles)
• Telangiectasias

47
Q

How do you diagnose GERD

A

Via treatment = PPI + lifestyle

48
Q

Tx of H. Pylori

A

Triple therapy: PPI + Clarithromycin (or metronidazole) + Amoxicillin

49
Q

How do you diagnose Zollinger-Ellison syndrome

A
  • Gastrin levels remain elevated even after administration of secretin, which normally inhibits gastrin release
  • Secretin paradoxically stimulates gastrin release from gastrinomas
50
Q

Tx of Zollinger-Ellison syndrome

A

Resection

MS3 (88 decks)

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