tests 22 Flashcards

0
Q

narcolepsy treatment

A

stimulants during the day (amphetamines, modafinil). nighttim sodium oxybate (GHB).

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1
Q

What is the chemical problem in narcolepsy?

A

not enough hypocretin (aka orexin) production by the lateral hypothalamus. these neuropeptides promote wakefulness and inhibit REM sleep-related phenomena. hypocretin-1 is measurable in the CSF (though not in narcoleptic people) but not in the serum.

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2
Q

Which immunoglobulins fix complement? What is the function of IgA and IgE?

A

IgM and IgG fix complement
IgA prevents attachment of bacteria and viruses to mucous membranes. it is a monomer in the circulation and a dimer when secreted.
IgE: binds mast cells and basophils. cross-links when exposed to antigen. mediates type I hypersensitivity. activates eosinophils.

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3
Q

Piriform recesses: where is it? relevant injuries?

A

small cavities on either side of the laryngeal orifice. they are bounded medially by the aryepiglottic folds and laterally by the thyroid cartilage and thyrohyoid membrane. a thin layer of mucosa overlying the piriform recess is all that protects the superficially coursing internal laryngeal nerve (branch of csuperior laryngeal nerve). It mediates cough reflex by carrying sensation from the mucosa superior to the vocal cords. it is easily injured when food gets stuck in the piriform recesses.

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4
Q

Describe normal gas exchange, including numbers

A
  1. ambient air has a pO2 around 160
  2. tracheal air has a pO2 around 150 (smaller because of partial pressure of water vapor).
  3. alveolar pO2 should be around 100 (or 104). This is the equilibration point between the pressure in the trachea and the pressure in venous blood (40). pCO2 in alveoli should be around 40 (between tracheal pressure- 0 mmHg- and venous pressure- 45 mmHg).
    If equilibration occurs at it should, it is perfusion limited (limited by how much blood can flow through the lungs). If perfusion is poor, equilibrium will occur slowly or may not occur at all.
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5
Q

treatment for S. epidermids

A

IV vancomycin with gentamicin or rifampin or both. S epidermidis is usually resistant to methicillin (and cephalosporins, etc).

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6
Q

How do you reduce the likelihood of confounding in case-control studies? How is it different from selection bias?

A

MATCHING based on potential confounders.

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7
Q

primary biliary cirrhosis vs. primary sclerosing cholangitis

A

primary biliary cirrhosis: autoimmune reaction that causes lymphocyte infiltration and periductal granulomas. It usually involves middle aged women and is insidious in onset. It may begin with hepatosplenomegaly, choelestasis, itchiness at night. increased serum mitochondrial antibodies. may have high IgM.

primary sclerosing cholangitis: onion skin bile duct fibrosis, with beading of intra and extra hepatic ducts on ERCP. associated with hypergammaglobulinemia (IgM) and ulcerative colitis. can lead to secondary biliary cirrhosis and cholangiocarcionma. often pANCA positive.

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8
Q

What heart sounds are associated with ASD? VSD?

A

ASD: loud S1; wide, fixed, split S2.
VSD: may be associated feta alcohol exposure. causes turbulent high velocity blood flow across a small VSD, producing a loud, holosystolic murmur heard over the left sternal border of the third or fourth intercostal space.
murmur may be absent if the VSD is big enough.

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9
Q

Integrins: function, binding partners

A

integrins are membrane proteins that maintain ibasolateral membrane integrity by binding to collagen and laminin in the basement membrane. they also bind fibronectin, which helps mediate cell adhesion and migration.

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10
Q

post strep glomerulonephritis histo

A

hypercellular, inflammed glomeruli on H and E.

mediated by immune complex deposition with subepithelial humps on EM.

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11
Q

How do you treat DKA?

A

give SHORT ACTING, regular insulin. (this takes longer to work than rapid acting but is the second fastest). it will be continuous, IV regular insulin. regular insulin starts working within 30 min, peaks at 2-4 hrs, and lasts 5-6 hours

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12
Q

Other than hepatocellular carcinoma, what are three other important liver tumors?

A
  1. cavernous hemangioma: most common benign liver tumor. thought to be a congenital lesion that expands via ectasia (dilation). histo shows cavernous, blood filled vascular spaces lined by a single epithelial layer. biopsy is contraidicated because of bleeding risk.
  2. hepatic adenoma: rare but benign tumor. related to OCPs or anabolic steroids. may regress spontaneously or rupture (causing shock and abdominal pain).
  3. angiosarcoma: malignant tumor of endothelial origin related to exposure to arsenic or vinyl chloride.
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13
Q

What does the femoral nerve do? How would an injury present?

A

femoral nerve innervates the muscles responsible for flexion of the thigh at the hip (iliacus and sartorius muscles) and extension of the leg at the knee (quadraceps). It also supplies sensory innervation to the skin on the anterior thigh and medial leg. injury causes loss of knee reflex and anterior thigh sensory loss.

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14
Q

What muscles and nerves are involved in the Trendelenberg sign?

A

remember, trendelenberg means that the the hip dips toward the unaffected side when the patient stands on the affected leg. it is usually due to weakness of the gluteus medius and gulteus minimus, which are supplied by the superior gluteal nerve.

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15
Q

congeintal torticollis

A

develops by 2-4 wks of age. caused by birth trauma (breech delivery) or by malposition of the head in utero. this causes sternocleidomastoid muscle injury and fibrosis. congenital torticollis may rarely be the result of cervical spine deformities. Kids with congenital torticollis bay also have hip dysplasia, metatarsus adductus, etc.

presentation: head tilted toward the affected side with the chin pointing away from the contracture. soft tissue mass may be palpable in the inferior 1/3 of the SCM.

16
Q

HMP shunt: biochemical, where in the cell does it happen, what are the blood smear findings for G6PD

A

2 phases:
1. oxidative: glucose 6-P to 6-phosphogluconate via G6PD enzyme (rate limiting step). 6-phosphogluconate goes to ribulose-5-phosphate. oxidative phase is irreverisble.
2. nonoxidative phase: basically allows you to put energy back into glycolysis.
all rxns occur in the cytoplasm.
G6PD deficient patients have HEINZ bodies and may cause erythrocyte deformation.

17
Q

How do you treat legionella

A

fluoroquinolones or newer macrolides

18
Q

What are the major muscles responsible for hip motion? What muscles do we use to sit up from the supine position?

A

flexion: iliopsoas, rectus femoris, tensor fascia lata
extension: gluteus maximus, biceps femoris- long head (semitendinosus, semimembranosus)
abduction: gluteus minimus and medius
adduction: adductor brevis, longus, and magnus.
to sit up from supine, we use the external abdominal obliques, the rectus abdominus, and the hip flexors.

19
Q

What are the types of gall stones and how are they different? What is the pathogenesis of brown gallstones?

A

Gallstones may be:
1. cholesterol: radiolucent with 10-20% opaque due to calcifications. Associated with obesity, Crohn’s, CF, age, clofibrate, esterogen, mutiparity, rapid weight loss, Native American origin.
2. Pigmented. Black stones are radiopaque and due to hemolysis. Brown stones are radiolucent and due to infection. Pigmented stones are seen in pts with chromic hemolysis, alcoholic cirrhosis, advanced age, and biliary infection.
In terms of infection: infection causes release of beta glucuronidase by injured hepatocytes and bacteria. this enzyme contributes to hydrolysis of bilirubin glucuronides and increases the amt of unconjugated bilirubin in bile. Infections include E. coli, ascaris lumbricoides, or Opisthorchis sinensis.

20
Q

What are some complications of gall stones?

A

cholecystitis, ascending cholangitis, acute pancreatitis, bile stasis, biliary colic.
Can also cause a fistula between the gallbladder and the small intestine, causing air in the biliary tree. Or, gallstone may obstruct the ileocecal valve and cause gallstone ileus.

21
Q

ganciclovir vs. foscarnet: MOA and side effects

A

both are used to treat CMV retinitis
ganciclovir requires viral activation. It is a guanosine analog that preferentially inhibits viral DNA pol. It can cause leukopenia, neutropenia, thrombocytopenia, and renal toxicity.
FOScarnet is pyroFOSphate analog that also acts as a viral DNA pol inhibitor. It binds to the pyrophosphate binding site of the enzyme. It does not require viral activation. However, it can cause nephrotoxicity, hypocalcemia, and hypomagnesemia (it is a pyrophosphate analog and can chelate Ca, cause renal Mg wasting, and decrease PTH).

22
Q

What are the key features of allergic bronchopulmonary aspergillosis?

A

seen in asthmatic and CF patients. aspergillis colonizes the the bronchial mucosa and causes a hypersensitivity reaction. patients have high serum IgE levels, EOSINOPHILIA, and IgE and IgG antibodies to aspergillus. There is AIRWAY INFLAMMATION and MUCUS PLUGGING with exacerbations and remissions. repeated exacerbations may produce PULMONARY INFILTRATES and proximal BROCHIECTASIS.

23
Q

What are causes of acute gastritis?

A

acute gastritis is caused by an imbalance between the factors that protect the mucosa (mucin layer made by foveolar cells, bicar secretion, and blood supply that picks up leaked acid and provides nutrients) and the acid.
May be caused by severe burns (curling ulcer: decr. blood supply), NSAIDs, heavy alcohol consumption (toxin damage), chemotherapy (reduced cell regeneration), increased intracrainal pressure (Cushing ulcer: incr. vagal stimulation causes incr. acid production), shock/stress.

24
Q

chronic autoimmune gastritis

A

autoimmune destruction of parietal cells in the body and fundus. see antibodies against parietal cells or intrinsic factor in blood. But, note that this is a T-CELL MEDIATED destruction (antibodies are useful for dx but don’t cause the disease). causes mucosal atrophy with intestinal metaplasia, achlorhydria, perinicious anemia, and an incr. risk of gastric adenocarcinoma.

25
Q

chronic H. pylori gastritis

A

found predominately in the ANTRUM. H pylori weakens mucosal defenses. presents with epigastric abdominal pain, incr. risk of PUD, incr. risk of intestinal type gastric carcinoma, and MALT lymphoma.

26
Q

What areas of the brain are most affected by Alzheimer’s disease?

A

in advanced AD, patients have diffuse brain atrophy, ESPECIALLY around the temporoparietal lobes and the hippocampus.
Hippocampal atrophy is evident even in the early stages of the disease.

27
Q

Which sympathetic receptors affect the eye and how? What about insulin and renin?

A

alpha 1: increases pupillary dilatro muscle contraction.
alpha 2: decreases insulin release, lipolysis. increase platelet aggregation
beta 1: increase renin release (and lipolysis)
beta 2: increase insulin release, ciliary muscle relaxation, and aqueous humor production

28
Q

What bacteria are associated with aspiration pneumonia? What about with penetrating chest trauma?

A

aspiration: peptostreptococcus and fusobacterium, or bacteroides. These are gram negative bacteria.
chest trauma: staph and strep; potentially E. coli and fungi.

29
Q

What are the functions of CNVII?

A
  1. motor output to facial muscles
  2. parasympathetic output to lacrimal glands, submandibular, and sublingual glands
  3. taste to anterior 2/3 of tongue
  4. somatic afferents from the pinna and external auditory canal; stapes muscle.
    patients with Bell’s palsy may have decr. tearing, hyperacusis, and/or loss of taste sensation over the anterior 2/3 of the tongue
30
Q

conversion disorder vs. somatization disorder

A

both disorders produce physical symptoms without identifiable physical causes and are UNCONSCIOUS.
somatization disorder: variety of complaints in one or more organ systems that last months-years. associated with excessive, persistent thoughts and anxiety about symptoms. May co-occur with medical illness.
conversion disorder: SUDDEN loss of sensory or motor function, often following an acute stressor. patient is aware of symptoms but is sometimes indifferent to them. More common in women, teens, and young adults.

31
Q

natural killer cells: how do they kill, what do they kill, cell surface markers, activation factors

A

they kill by using perforin and granzymes to induce apoptosis of virally infected cells and tumor cells. they can also kill via antibody-dependent cell-mediated cytotoxicity.
they are mainly activated by IL-12 and IFN-gamma (though also by IL-2 and other IFNs).
they express CD16 or CD56.