Internal Med 11 Flashcards
Tx of urethritis
- Almost always STD (Gon/Chla)
- Tx = CTX + Azithro or Doxy
- HIV screen
Tx of asymptomatic bacteruria
- Only treat if pregnant or with urinary procedure
* Tx in pregnancy = Amoxicillin
Tx of uncomplicated cystitis
o Empiric: TMP/SMX, Nitrofurantoin, Fosfomycin
o 3 days
Tx of complicated cystitis
o Empiric: TMP/SMX, Nitrofurantoin, Fosfomycin
o 7 days
Tx of pyelonephritis
o IV = CTX
o PO = Cipro
o 10 days
Tx of perinephric abscess
o I&D
o Abx same as pyelo but for longer
♣ CTX
o 14 days
What are the major criteria of Endocarditis
- Bacteremia
- New regurg murmur
- Vegetations on echo
What are the minor criteria of endocarditis
- Risk factors (IV drug use, h/o endocarditis, prosthetic valve)
- Fever >38
- Vascular complications (splinter hemorrhages, janeway lesions)
- Rheumatologic complications (Osler nodes, glomerulonephritis)
Tx of endocarditis
Abx for 4-6 weeks
♣ Native valve
• Vancomycin
♣ New prosthetic valve (<60 days)
• Vanc + Gent + Cefepime
♣ Old prosthetic valve (>365 days)
• Vanc + Gent + Ceftriaxone
When do you get surgery for endocarditis
- Pt has developed CHF
- Vegatation >15 mm
- Vegetation >10 mm with embolism
- Abscess (abx won’t work)
- Fungus
What does Hyperkalemia do to EKG
- Peaked T-waves
* Then everything gets stretched out (PR interval prolonged, widened QRS, torsades)
What does hypokalemia do to EKG
Prolonged QT, flattened T-waves, U-waves
What does hypocalcemia do to EKG
On EKG: prolonged QTc
What does hypercalcemia do to EKG
On EKG: shortened QTc
What is Zosyn
Pip/Tazo
What is Unasyn
Amp/Sul
What is Augmentin
Amox/Clav
Is the TSH likely to be high or low in thyroid cancer
High - thyroid cancers are usually NOT hyperfunctioning (no hyperthyroidism in cancer)
What will you see in papillary thyroid carcinoma
• Histology:
o Orphan Annie eye nuclei
o Nuclear grooves
o Psammoma bodies
What will you see in follicular thyroid carcinoma
• 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)
What will you see in medullary thyroid carcinoma
- 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)
How might diabetes affect the GI tract
Diabetic autonomic neuropathy of the GI tract (e.g. delayed gastric emptying)
How do you treat diabetic gastroparesis
Metoclopramide (D2 receptor antagonist) has prokinetic and antiemetic effects
What will you see in the fluid of a loculated pleural fluid collection caused by pneumonia
- Glucose
- pH
- protien
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
What is the most effective non-pharmacologic measure to decrease BP
Weight loss
What is the first step in someone with Cushing’s syndrome
Cushing syndrome = increased cortisol
First step is to measure ACTH
What does Cushing syndrome + low ACTH mean
Adrenal tumor or exogenous glucocorticoids
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
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
What is Addison disease
♣ Primary adrenal insufficiency problem of the adrenal gland
• Most commonly due to autoimmune destruction of adrenal gland
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)
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
What is Conn Syndrome
♣ Primary hyperaldosteronism:
• Aka Conn syndrome
• Due to adrenal adenoma
• Will see decreased renin due to negative feedback
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+
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)
Causes of secondary hyperaldosteronism
o Renal artery stenosis
o Congestive heart failure
o Low protein states (decreased osmotic pressure leads to low blood volume)
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
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
Will sodium be high or low in DKA
o Hyponatremia due to sodium loss via diuresis (osmotic diuresis due to increased glucose)
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
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
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
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
What are the infectious causes of esophagitis
- Candida
- HSV
- CMV
- HIV
Tx of eosoniphilic esophagits
- PPI
- If PPI does not fix problem, then give aerosolized steroids
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
How do you diagnose GERD
Via treatment = PPI + lifestyle
Tx of H. Pylori
Triple therapy: PPI + Clarithromycin (or metronidazole) + Amoxicillin
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
Tx of Zollinger-Ellison syndrome
Resection
