Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

MS3 > Internal Med 11 > Flashcards

Internal Med 11 Flashcards

(50 cards)

Start Studying
1
Q

Tx of urethritis

A
  • Almost always STD (Gon/Chla)
  • Tx = CTX + Azithro or Doxy
  • HIV screen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Tx of asymptomatic bacteruria

A
  • Only treat if pregnant or with urinary procedure

* Tx in pregnancy = Amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tx of uncomplicated cystitis

A

o Empiric: TMP/SMX, Nitrofurantoin, Fosfomycin

o 3 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Tx of complicated cystitis

A

o Empiric: TMP/SMX, Nitrofurantoin, Fosfomycin

o 7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Tx of pyelonephritis

A

o IV = CTX
o PO = Cipro
o 10 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Tx of perinephric abscess

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the major criteria of Endocarditis

A
  • Bacteremia
  • New regurg murmur
  • Vegetations on echo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What does Hyperkalemia do to EKG

A
  • Peaked T-waves

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does hypokalemia do to EKG

A

Prolonged QT, flattened T-waves, U-waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does hypocalcemia do to EKG

A

On EKG: prolonged QTc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does hypercalcemia do to EKG

A

On EKG: shortened QTc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Zosyn

A

Pip/Tazo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Unasyn

A

Amp/Sul

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is Augmentin

A

Amox/Clav

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What will you see in papillary thyroid carcinoma

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What will you see in medullary thyroid carcinoma

Study These Flashcards
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

Study These Flashcards
A

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

23
Q

How do you treat diabetic gastroparesis

Study These Flashcards
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
Study These Flashcards
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
What is the most effective non-pharmacologic measure to decrease BP
Weight loss
26
What is the first step in someone with Cushing's syndrome
Cushing syndrome = increased cortisol First step is to measure ACTH
27
What does Cushing syndrome + low ACTH mean
Adrenal tumor or exogenous glucocorticoids
28
What is the next step if Cushing syndrome + high ACTH
Now you suspect Cushing disease (ACTH-pituitary adenoma) or ectopic ACTH secreting tumor Need to do a high dose Dexamethasone suppression test
29
Describe results of high dose dexamethasone suppression test
♣ Cortisol levels will decrease if Cushing Disease (ACTH-pituitary adenoma) ♣ Cortisol levels will remain elevated if ectopic tumor
30
What is Addison disease
♣ Primary adrenal insufficiency problem of the adrenal gland • Most commonly due to autoimmune destruction of adrenal gland
31
Presentation of Addison disease
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
Describe presentation of Secondary adrenal insufficiency
♣ 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
What is Conn Syndrome
♣ Primary hyperaldosteronism: • Aka Conn syndrome • Due to adrenal adenoma • Will see decreased renin due to negative feedback
34
Describe presentation of Hyperaldosteronism
• 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
How do you distinguish Primary hyperaldosteronism from secondary hyperaldosteronism
Primary = will have decreased renin due to neg feedback Secondary = high renin (this is the primary problem)
36
Causes of secondary hyperaldosteronism
o Renal artery stenosis o Congestive heart failure o Low protein states (decreased osmotic pressure leads to low blood volume)
37
Tx of pheochromocytoma
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
Describe pathogenesis of DKA
• 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
Will sodium be high or low in DKA
o Hyponatremia due to sodium loss via diuresis (osmotic diuresis due to increased glucose)
40
Will potassium be high or low in DKA
• 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
Tx of DKA
• 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
What is the major complication of Type 2 DM
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
What will you see in blood sugar, ketones, and pH in HHNS
♣ 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
What are the infectious causes of esophagitis
- Candida - HSV - CMV - HIV
45
Tx of eosoniphilic esophagits
- PPI | - If PPI does not fix problem, then give aerosolized steroids
46
What are the symptoms of scleroderma
♣ CREST syndrome: • Calcinosis (calcium deposition) / anti-centromere antibody • Raynoud • Esophageal dysmotility • Sclerodactyly (tightening of skin with loss of wrinkles) • Telangiectasias
47
How do you diagnose GERD
Via treatment = PPI + lifestyle
48
Tx of H. Pylori
Triple therapy: PPI + Clarithromycin (or metronidazole) + Amoxicillin
49
How do you diagnose Zollinger-Ellison syndrome
* Gastrin levels remain elevated even after administration of secretin, which normally inhibits gastrin release * Secretin paradoxically stimulates gastrin release from gastrinomas
50
Tx of Zollinger-Ellison syndrome
Resection

MS3 (88 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions