MSKAP 1 Flashcards
Tx for strep pyogenes necrotizing fasciitis
Group A strep nec fasc tx with combo PCN + clinda (suppresses strep toxic production)
Pathogenesis of acute interstitial nephritis
Immune cell infiltration of kidney interstitium
Describe how tx with estrogen for metastatic prostate cancer can induce hypocalcemia
Bony mets of prosate CA act as calcium sink inducing serum hypocalcemia
Estrogen inhibits bone resorption unmasking the increase in bony Ca uptake by mets
Indication for adrenal vein sampling
Adrenal vein used to lateralize abnormal adrenal hormone secretion
Class I vs. II of pHTN
Class I pHTN = idiopathic
Class II pHTN = PAH 2/2 L heart failure (HFrEF, HFpEF)
Physiologic vs pathologic split in S2
Physiologic (normal) for S2 to split during inspiration (increased preload 2/2 increased intrathoracic pressure)
Paradoxical/pathologic split of S2 is present during expiration- due to delay in LV emptying (A takes even longer to close) due to severe aortic stenosis
-so presence of S2 in inspiration is helpful for ruling OUT severe AS
What is porphyria cutanea tarda?
(a) Main clinical manifestation
Porphyria cutanea tarda = skin manifestations of acquired deficiency in liver enzyme required for heme synthesis
-prompts accumulation of porphyrins that are photosensitive
(a) Photosensitive prophyrins mvoed to skin where the disrupt the epidermal barrier => fragile skin and blisters on sun exposed areas
What is hungry bone syndrome?
(a) Lab abnormalities?
Hungry bone syndrome: no PTH to tell bones to breakdown (aka after parathyroidectomy) so bone acts a sink for calcium, phos, and mag
(a) Low Ca, phos, and mag (all hypo)
Differentiate causes of types of bone pain in elderly:
osteomalacia vs. osteitis fibrosis cystica
Bony pain
-osteomalacia due to vitamin D deficiency (no sunlight or poor gut absorption from diet etc)
vs
-osteitis fibrosis cystica is due to long-standing exposure to very elevated PTH (ex: primary hyperparathyroidism or secondary from kidney disease): bony pain and typical subperiosteal bone resorption pattern on Xrays
Serum coag results in pt w/ vitamin K deficiency
- elevated PT/INR (b/c PT is more sensitive to reduction in factor VII levels and vit K needed to make 1972)
- normal PTT
Describe classification staging of pulmonary fibrosis
Radiographically classified (not by symptoms) b/c correlates w/ % spontaneously resolve w/o treatment
I- hilar lymphadenopathy w/ normal lung parenchyma (> 90%)
II- hilar LN w/ abnormal parenchyma (~50% spontaneously improve w/o tx)
III- no hilar LN but abnormal parenchyma (~20%)
IV- extensive parenchymal changes w/ fibrosis and architectural distortion
Adult M admitted for HF exacerbation found to have central sleep apnea w/ Cheyne-Stokes breathing pattern
First line tx?
First line tx for heart failure related central sleep apnea = optimizing HF therapy (ex: furosemide…)
-degree of central sleep apnea often correlates w/ LV dysfunction
Not CPAP! that would be for OSA, while central sleep apnea is cheyne-stokes w/ ABSENCE of upper airway obstruction
Mechanism of roflumilast vs. theophylline
Both are phosphodiesterase inhibitors, roflumilast (decreases exacerbations) is PDE5 specific
Theophylline is a nonspecific phosphodiesterase inhibitor => bronchodilator
Clinical features that distinguish serotonin syndrome from NMS
Serotonin syndrome- faster onset (hours) and faster resolution (24 hrs). 2/2 overdose of serotonin agents. +fever, hyperreflexia, myoclonus
NMS- more subacute (days/weeks) onst and takes longer to resolve (Days/weeks). 2/2 uptitration of antipsychotics or removal of Parkinsonian (dopaminergic) agent.
+higher fever, hyporeflexia, rigidity
Describe 2 expected lab abnormalities seen in cyanide poisoning
Cyanide poisoning inhibits intracellular oxidative phosphylation => no aerobic respiration
- Lactic acidosis
- Abnormally elevated central venous O2 (b/c O2 not being used in tissues…)
ADA guidelines for normal
(a) fasting BS
(b) 2-hr postprandial BS
(a) 80-130
(b) under 180
Scenario of cyanide poisoning
(a) Mechanism of poisoning
Cyanide poisoning- fire
(a) Inhibits intracellular oxidative phosphorylation => can only do anaerobic metabolism => tissues don’t get ATP => multisystem organ failure
Risk factors for porphyria cutanea tarda
Risk factors for porphyria cutanea tarda (acquired liver enzyme deficiency causing accumulation of porphyrins) EtOH Smoking Hep C HIV
Thought to be 2/2 increased oxidative stress to liver or somehow reduced hepcidin expression (which increases iron absorption)
Type 1 vs. Type 2 autoimmune pancreatitis
AIP
Primary- part of a systemic IgG4-positive disease
vs.
Secondary- granulocytic lesions without IgG4-positive cells or systemic involvement
Indications for cinacalcet treatment
Cinacalcet increases sensitivity of parathyroid gland receptors to calcium => reducing PTH secretion
Use in secondary parathyroidism 2/2 CKD to reduce hypercalcemia from bone breakdown
Proposed mechanism by which IV Mag reduces admission for acute asthma exacerbation
Bronchial dilation
Differentiate type I vs type II amiodarone induced thyrotoxicosis
(a) How to differentiate on thyroid ultrasound
(b) Differing treatments
Amiodarone induced thyrotoxicosis (hyperthyroidism in s/o amio)
Type I- underlying Graves or hyperplasia, so with big increase of substrate (amio has 2 iodine components per compound) thyroid becomes super hyperactive
(a) increase flow/vascularity on doppler ultrasound
(b) tx w/ methimazole
Type II- no underlying disease, amio can directly cause destructive folliculitis (rupture of follicular cells releases stored thyroid hormone)
(a) No increased vascularity on ultrasound
(b) Steroids as tx
Definition of acute IPF exacerbation
IPF exacerbation: less than 30 days of worsening dyspnea with new diffuse GGOs on top of pre-existing imaging findings (typically bibasilar fibrotic changes w/ extensive honeycombing)
Thyroid cancer
(a) Most common
(b) From parafollicular cells
Thyroid cancer
(a) 85% are papillary, next 10% follicular, 3% medullary
(b) Medullary thyroid cancer- from parafollicular cells, seen in MEN 2A/2B
Dog bite
(a) What bacteria to expect if gets infected
(b) When to give abx
(c) Which abx
Dog bite- (a) expect skin flora and polymicrobial- staph, strep, bacteroides, pasteurella
(b) any immuncompromised state including asplenia, cirrhosis
(c) Augmentin (amox-clavulanate)
Inciting factors of
(a) NMS
(b) Serotonin syndrome
(c) Malignant hyperthermia
Inciting factors
(a) Neuroleptic malignant syndrome: mostly from antipsychotics (haldol, risperidol etc) also antiemetics (reglan)
(b) Serotonin syndrome from 2+ agents that affect release/reuptake of serotonin: ex: SSRI and ecstasy
(c) Malignant hyperthermia due to inhaled anesthetic (halothane, isoflurane) or depolarizing paralytic (succinylcholine)
Pt w/ hypereosinophilic asthma and nasal polyps may want to avoid what class of meds?
Semter’s triad: severe asthma, hyperplastic nasal polyps w/ eosinophilia, aspirin sensitivity
=> avoid COX1 inhibitors = ASA and NSAIDs
2 treatment regimens for LTBI in HIV negative pt
(a) INH daily, self administered, for 9 months
b) INH and rifapentine weekly for 12 weeks (not 24 weeks…), has to be DOT (as w/ all intermittent regimens
Expected adjustment to levothyroxine dose for pt starting tamoxifen or estrogen
Tamoxifen/estrogen increases thyroid binding protein => reduces free circulating thyroid hormone
So increase levothyroxine dose when starting estrogen compound (vs. decrease when start testosterone)
Pt w/ proven scabies s/p 2 doses of permethrin, still w/ itching but no new lesions
Next step in management?
Tx symptoms of itching (benadryl, topical low-dose steroid) but don’t need to do permethrin or oral ivermectin unless new lesions accumuating
Not uncommon to see post-tx persistent itching
What is actigraphy?
Actigraphy = wrist monitor for sleep cycle, duration
-more accurate version of a slepe diary
Pemphigus vulgaris vs. Bullous pemphigoid
a) Nikolsky sign
(b) H&E stain (where is the clefting?
Pemphigous vulgaris: flaccid blisters + mucus membrane involvement
(a) + Nikolsky sign
(b) Suprabasilar clefting (more superficial than in BP)
Bullous pemphigoid: tense blisters, no mucus membrane involvement
(a) Negative Nikolsky
(b) Subepidermal clefting
74 y/oF presents w/ symptomatic hypocalcemia shortly after starting alendronate-
what other hormone should be measured?
Vitamin D- needs to be measured and stores replete before starting any bisphosphonate
Bisphosphonate inhibits osteoclast activity, if there is underlying vit D deficiency (active vitamin D works on bone to regulate serum Ca levels) then at high risk of hypocalcemia
Mainstay of treatment for serotonin syndrome
Treat autonomic instability w/ supportive care and benzos
Essentially overdose of drugs that affect reuptake/release of serotonin (ex: ecstasy, SSRI)
Class II vs. III of pHTN
Class II and III are due to cardiac and pulmonary causes, respectively
class II pHTN = PAH 2/2 elevated L sided pressures (HFrEF, HFpEF)
class III pHTN = PAH 2/2 lung disease or chronic hypoxia (COPD, IPD/ILD)
Pre-op BP management of pheo removal
(a) First line class of drugs
Pre-op management for pheo removal: 10-15 days pre-op start alpha blocker to prevent hypertensive crisis (seen due to catechol surge w/ anesthesia induction or tumor manipulation)
(a) Phenoxybenzamine = alpha receptor blocker
What is erythrasma?
(a) Tx
Erythrasma = bacterial (gram positive) infection of intertriginous area (groin, folds)
(a) Tx- topical clinda/erythromycin
2 indicated tests for pt w/ incidentally found adrenal mass
Incidental adrenal mass: want to r/o pheo and subclinical Cushing’s syndrome
- 24-hr urine free metanephrines to r/o pheo
- 1mg dexamethasone suppression test (normal would be AM serum cortisol <5) to r/o subclinical Cushing’s
Mainstay of treatment for NMS vs. malignant hyperthermia
Treatment:
NMS (from antipsychotic or withdrawal of dopaminergic agent): stop triggering event (hold antipsychotic, reuptitrate withdrawn Parkinson med)
-poor data for dantrolene
-after ~2 weeks can reintroduce antipsychotic at lower dose
Malignant hyperthermia (from inhaled anethetic or succ in genetic susceptible pt)- stop agent, active cooling, dantrolene IV q5-10 minutes
Pemphigus vulgaris vs. Bullous pemphigoid
(a) Type of blister
(b) Location/skin involvement
Pemphigus vulgaris
(a) flacid, painful blister b/c more superficial
(b) involves mucus membranes, especially the mouth
Bullous pemphogoid
(a) tense blisters b/c deeper (subepidermal antibody), often itchy
(b) typical no oral lesions, mucous membrane involvement less likely
CSF studies expected in tuberculosis meningitis
Tb/fungal meningitis:
- clear color
- WBCs elevated but < 500 (not in thousands like bacterial)
- Protein moderately elevated like 45-200 (viral under 200, bacterial over 200)
- glucose normal to low, in Tb typically under 40 (low like bacterial vs. normal in viral)
55 y/oF smoker should get which pneumococcal vaccine?
PPSV23 has a much broader base for pts under 65: includes immunosuppression but also many chronic diseases (DM, heart, liver, kidney) and smokers
PCV13 only for under age 65 in immunocompromised (asplenia)
Mechanism of bosentan in pHTN
Bosentan = endothelin receptor antagonist
-endothelin found on vascular smooth muscle and bronchioles, when activated causes vasoconstriction
Key lab abnormality in granulomatous disease that leads to hypercalcemia
Elevated 1,25-OH vit D b/c macrophages in the granuloma activate 25-OH to 1,25-OH in a PTH-independent manner (while kidneys will listen to PTH)
So high serum 1,25-OH vit D will stimulate Ca2+ and phos absorption (from gut and bone) => hypercalcemia
(ex: so in pt w/ CXR c/f sarcoid, measure 1,25-OH D instead of PTHrP to determine mechanism of hypercalcemia)
Mechanism of action of micafungin
Micafungin inhibits 1-3-beta-D-glucan synthase, an essential polysaccharide for candida cell wall
decreased glucan content causes osmotic instability and cellular lysis
=> micafungin is first-line tx for candidemia/invasive candidiasis
Main pharmacologic agent for treating acute hep B
Acute hepatitis B- typically will self-resolve, only ~1% progress to liver failure and 5% progress to chronic hepB
Tx first line = nucleot(s)ide analogs tenofovir and entecavir
Phenoxybenzamine
(a) Mechanism
(b) Main indication in pheo pre-surgical management
Phenoxybenzamine
(a) Alpha receptor blocker- causes peripheral venodilation (opposite of pressors)
(b) Alpha blockade to prevent hypertensive crisis peri-op for pheo removal
- huge catechol surge during anesthesia induction and tumor manipulation: uptitrate alpha blockade to goal systolic under 130 pre-op
First line tx for actinic keratosis
Topical 5-FU
5-FU inhibits rapidly replication cells
Pathogenesis of how amyloidosis causes proteinuria
Amyloidosis = plasma cell dyscrasia where light chain (kappa and lambda) are deposited in end organs causing damage
27F w/ Graves started on methimazole 3 months ago p/w fever, sore throat, pain w/ swallowing
In addition to supportive care what else is required?
Need to rule out methimazole-induced agranulocytosis
Methimazole can cause bone marrow suppression => get CBC to calculate ANC
Diagnostic criteria for CTEPH
CTEPH diagnosis:
(1) pHTN (R sided pressures) over 25 mmHg w/o elevated L-sided pressures
+
(2) imaging findings of chronic thromboembolism
pulmonary arterial webbing, luminal irregularities/narrowing
Indications for tacrolimus
(a) Topical
(b) Systemic
Tacrolimus = non-steroid immunomodulator, works as calcineurin inhibitor to inhibit T-cell activation
(a) Topically used as second line agent for atopic dermatitis
(b) Systemically used in post-transplant patients (ex: prevention of G vs host disease)
Also in fistulating Crohns, refractory rheumatoid arthritis
Mechanism of hypothryoidism in late stages of subacute thyroiditis
Subacute thyroiditis- painful destruction of thyroid follicular cells => release stored thyroid hormone
2-6 weeks of hyperthyroid, followed by 6-12 weeks of hypothyroid after thyroid hormone stores are deplete
-may require transient levothyroxine
When to increase levothyroxine dose for hypothyroid pregnant F
Immediately once pregnancy confirmed
T4 requirements increase by 40-50% from TSH/HCG rather quickly, so don’t want until 3rd trimester
Differentiate amyopathic dermatomyosis and dermatomyositis
Dermatomyositis = autoimmune against skin and proximal muscles
“a-myopathic” (without muscle) has the cutaneous findings (Gottrons papules, shawl sign, heliotrope rash) with normal strength and normal muscle enzymes
What is dermatomyositis?
Dermatomyositis = autoimmune against skin and proximal muscle
- muscle weakness, elevated CK
- skin: Gottron’s papules (lichenoid patches on knucles), shawl sign, heliotrope rash (on eyelides)
Etiologies of cavernous sinus thrombosis
Clot in intracranial vein
- acquired hemophilia (OCPs, pregnancy, malignancy)
- inherited hemophilia (genetic)
- HEENT infection (S. Aureus)
Why measure alk phos prior to starting bisphosphonate after radiographic dx of Paget’s disease
B/c alk phos can be normal, indicating quiescent or burnt out phase of disease- during which bisphosphonates aren’t indicated/won’t help
Risk factors for vitamin K deficiency in hospitalized pts
- poor PO intake
- antibiotics (since most of vitK made from saprophytic bacteria in the colon)
- pancreatic dysfunction (fat-soluble vitamin)
74F w/ osteoporosis on alendronate x5 yrs
recent BMD: t-score -2.2 L-spine, -2.4 femoral neck
Next step in management?
Next step after 5 years of alendronate therapy in pt w/ non-severe osteoporosis (T score greater than -3.5) is to stop alendronate
-FLEX trial showed not much benefit of continuing alendronate for 10 vs. 5 yrs
Class II vs. IV of pHTN
Class II pHTN = PAH 2/2 L heart failure (HFrEF, HFpEF)
Class IV = PAH 2/2 pulmonary artery obstruction (ex: CTEPH)
vs. class III = PAH 2/2 lung disease or chronic hypoxia
Antibodies in Graves vs. Hashimotos
Graves (hyperthryoid): anti-thyrotropin receptor Abs
Hashimotos (autoimmune hypothyroid): anti-TPO (thyroid peroxidase) antibodies
Antimicrobial regimen of choice for
(a) cryptococcal meningitis
(b) candidema
(a) liposomal amphotericin B + flucytosine
(b) micafungin
Lab value findings of gestational thyrotoxicosis
HCG and TSH have the same alpha-subunit so some cross over => see elevated T4, with resultant suppressed TSH
High T4, low TSH
Downfall (limitation) of meningococcal vaccine
Vaccine doesn’t cover serogroup B which causes 40% of meningococcal meningitis
Higher risk of hypoglycemia: metformin vs. glyburide
Glyburide (sulfonylurea, stimulates insulin secretion from pancreas regardless of serum glucose) carries relatively high risk of hypoglycemia
Other sulfonylureas = glipize, glimepiride
Clinical presentation (onset of menses) that distinguishes Turner’s syndrome from primary ovarian insufficiency
Turner’s syndrome (X,0) presents in late teens w/ primary amenorrhea
Primary ovarian insufficiency- presents in 30/40s w/ secondary amenorrhea (pts stop getting their period, despite FSH levels elevated)
For treatment of myxedema coma which hormone should be given first?
Myxedema coma treatment: give IV hydrocort thennnn give IV levothyroxine
-if give thyroid hormone first may precipitate adrenal crisis due to augmented cortisol metabolism