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