Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Boards > Subjects 0321 > Flashcards

Subjects 0321 Flashcards

1
Q

How does carotid massage affect HR?

A

Increases pressure on carotid sinus –> more stretch –> more firing –> increase in AV node refractory period –> decr HR.

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

What is the Cushing reaction and how does it affect the autonomic system?

A

Triad: hypertension, bradycardia, respiratory depression
Incr ICP leads to compression of cerebral arterioles –> cerebral ischemia –> incr pCO2 and decr pH –> central reflex sympathetic incr in perfusion pressure (HTN) –> incr stretch –> incr peripheral reflex baroreceptor induced-bradycardia.

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

What are the blue baby congenital heart diseases? What increasing the shunting?

A

5T’s: truncus arteriosus, transposition, tricuspid atresia, tetralogy of falot, TAPVR.
The right-to-left shunts cause early hypoxia, so the patients manifest cyanosis in early childhood, or even at birth.
Generally, right-to-left shunts result from a high pulmonary venous resistance and low systemic vascular resistance. Increased pulmonary vascular resistance (PVR) (crying, hypoventilation, and acidosis) or decreased systemic peripheral resistance (SVR) (hypotension, histamine release, sepsis) will increase the shunting and worsen the hypoxia.

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

Drug induced lupus

A

SHIPP = Sulfonamides, hydralazine, isoniazid, procainamide, phenytoin

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

Hypertensive drugs for pregnant mothers?

A

Hypertensive Moms Love Nifedipine
-Hydralazine, methyldopa, labetalol, nifedipine

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

What are the two types of arteriolosclerosis?

A
  1. Hyaline: thickening of vessel walls in essential HTN or DM. 2. Hyperplastic: onion skinning in severe HTN with proliferation of smooth muscle cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do you characterize temporal arteritis?

A

Giant cell arteritis–focal granulomatous inflammation (with giant cells) characterize this process. Branches of carotid system are most often involved. Can lead to irreversible blindless if it involves ophthalmic artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Maple syrup urine disease is characterized by the defective breakdown of what?

A

I Love Vermont’s branched chain AAs. Defect in breadown of branched chain AA’s = Leucine, Isoleucine, and Valine. Degradation involves transamination to their respective a-ketoacids, which is then metabolized by branched-chain a-ketoacid dehydrogenase. Mutation in any 4 genes coding for 3 catalytic subunits.

Neurotoxicity results from accumulation of leucine in the serum and tissues. A metabolite of isoleucine gives the urine a sweet odor. MSUD can be life-threatening if untreated.
***Branched chain a-ketoacid dehydrogenase (similar to pyruvate and a-ketoglutarate dehydrogenase) requires the Tender Loving Care For Nobody co-enzymes = Thiamine pyrophosphate, Lipoate, Coenzyme A, FAD, NAD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Surface ectoderm

A

Rathke’s pouch (ant pit), lens, cornea, inner ear sensory organs, olfactory epithelium, nasal and oral epithelial linings, epidermis, salivary, sweat, mammary glands.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Neural tube –> ?

A

Brain and spinal cord, posterior pituitary, pineal gland, retina

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

Neural crest –> ?

A

Autonomic, sensory, celiac ganlia, schwann cells, pia and arachnoid mater, aorticopulmonary septum & endocardial cushions, branchial arches (bone and cartilage), skull bones, melanocytes, adrenal medulla.

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

Fragile X sydrome

A

Mild to moderate mental retardation, speech/language delay, autistic behavior and ADHD. Long face, prominent jaws, large ears, cleft palate. Macroorchidism. Mitral valve prolapse. Short height, joint laxity, scoliosis, pes cavus, double-jointed thumbs, single palmar crease.
***Increase in number of trinucleotide repeats in FMR1 gene on X-chromosome.

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

p-ANCA (perinuclear, anti-myeloperoxidase)

A

Microscopic polyangiitis: lung, kidney, skin (no nasopharyngeal), pauci-immune glomerulonephritis, palpable purpura.
Churg-Strauss (eosinophilic granulomatosis with polyangiitis): asthma, sinusitis, skin nodules or purpura, peripheral neuropathy (wrist/foot drop). Involves heart, GI, kidneys (pauci-immune).

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

What are the mRNA stop codons?

A

UGA, UAA, UAG. You go away, you are away, you are gone.

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

CN- toxicity

A

Sodium nitratate: promotes methemoglobin formation, which combines with CN- to form cyanmethemoglobin
Sodium thiosulfate: serves as sulfur donor to promote hepatic rhodanese-mediated conversion of CN- to thiocyanate, which is excreted in the urine.
Hydroxocobalamin: cobalt moiety binds to intracellular cyanide ions and forms cyanocobalamin, which is excreted in the urine.

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

Hep A inactivation

A

Water chlorination, bleach, formalin, UV irradiation, boiling for 85C for 1 min.

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

Describe the midgut development.

A

The midgut herniates through the umbilical ring at the 6th week of embryonic development to allow the rapid growth of the intestine and liver despite the slower growth of the abd cavity. The midgut returns to the cavity at 10th week of fetal life, and completes a 270 degree turn counterclockwise around the SMA.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the associated nerve injuries for: carpal tunnel, hook of the hamate, surgical neck of the humerus, head of radius, coracobrachialis?

A

Carpal tunnel: median nerve compression. Difficulty with fine motor control of thumb.
Hook of hamate: ulner nerve, near Guyon’s canal and pisiform bone in wrist
Medial epicondyle of humerus: ulner nerve
Fracture of surgical neck of humerus: axillary nerve –> paralysis of deltoid and teres minor, loss of sensation of lateral upper arm.
Radial head subluxation: deep branch of radial nerve –> weakness/paralysis of extensor compartment of forearm.
Coracobrachialis: lies deep to biceps brachii and overlies median nerve and brachial artery, innervated by musculocutaneous nerve.

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

What is Chediak-Higashi syndrome?

A

Chediak-Higashi syndrome is an autosomal recessive d/o of neutrophil phagosome lysosome fusion. Abnl giant lysosomal inclusions visible on light microscopy of a peripheral blood smear.

  1. Neurologic abnl (nystagmus, peripheral and cranial neuropathies)
  2. Partial albinism (abnl melanin storage in melanocytes)
  3. Immunodeficiency (defective neutrophil function, recurrent pyogenic infxn, staph + strep)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which bacteria produce IgA protease?

A

Neisseria meningitidis, N gonorrhoeae, S pneumoniae, H influenzae

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

Ureters in relation to gonadal vessels and common/external ilaic vessels?

A

Ureters cross over the common/external iliac vessels and under the gonadal vessels (and uterine vessels in females). They lie anterolateral to the internal iliac vessels and medial to the ovarian vessels within the true pelvis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What does the thayer-martin selection medium contain?

A

Chocolate (head blood) agar contains vancomycin (inhibit G+), colistin (polymyxin, inhibit G-), nystatin (inhibit fungi), and trimethoprim (G-, Proteus). Used to ID neisseria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Alpha-helices are found where in the cell?

A

Integral membrane proteins contain transmembrane domains composed of alpha helices with hydrophobic AA residues (valine, alanine, isoleucine, methionine, phenylalanine).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where are the following tumors located?
Craniopharyngioma:
Germ cell tumor:
Meningioma:

A

Craniopharyngioma: arise from remnants of Rathke’s pouch, located in suprasellar region. Present with hypothalamic or pituitary dysfunction and chnages in vision due to disruption of optic chiasm (bitemporal hemianopia).
Germ cell tumors: arise from pineal gland, located in dorsal midbrain. Cause obstructive hydrocephalus with sx of increased intracranial pressure (HA, vomiting, AMS), and Parinaud syndrome (upward gaze palsy).
Meningioma: falcine/parasagittal region over convexities of cerebral hemispheres. Most are disovered incidentally. Some have seizures, HA, forcal neuro deficits.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which hormones are secreted from the following structures?
Nucleus cereleus
Raphe nuclei
Nucleus basalis of Meynert
Red nucleus
Caudate nucleus and putamen
Substatia nigra

A

Nucleus ceruleus: NE-secreting neurons, fight or flight, dorsal pons
Raphe nucleus: Serotonergic relesasing neurons, midbrain, pons, and medulla, axons throughout CNS, sleep-wake cycle, level of arousal. Lesions: insomnia and depression.
Nucleus basalis of Meynert: cholinergic neurons. Alzheimer patient’s neurons here secrete inadequate amounts of acetylcholine.
Red nucleus: anterior midbrain, motor coordination of upper extremities.
Caudate nucleus and putamen: motor activities. Huntington’s–loss of cholinergic and GABA-releasing neurons in striatum.
Substantia nigra: dopaminergic neurons. Parkinson’s–depleted.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Ventromedial hypothalamic nuclei

A

Satiety. Destruction: hyperphagia. Stimulated by leptin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Lateral hypothalamic nuclei

A

Hunger. Destruction: anorexia. Inhibited by leptin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Anterior hypothalamic nuclei

A

Heat dissipation via parasympathetics. Destruction: hyperthermia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Posterior hypothalamic nuclei

A

Heat conservation via sympathetics. Destruction: hypothermia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Arcuate hypothalamic nuclei

A

Secretion of dopamine (inhibits prolactin), growth hormone-releasing hormone and gonadotropin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Paraventricular hypothalamic nuclei

A

Antidiuretic hormone, corticotropin-releasing hormone, oxytocin and thyrotropin-releasing hormone secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Supraoptic hypothalamic nuclei

A

Secretion of ADH and oxytocin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Suprachiasmatic hypothalamic nuclei

A

Circadian rhythm regulation and pineal gland function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Leucovorin

A

Or called folinic acid. Tx methotrexate overdose.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Filgrastim

A

G-CSF analog used to stimulate proliferation and differentiation of granulocytes in patients with neutropenia post-chemo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Cyclophosphamide toxicity

A

Hemorrhagic cystitis–use mesna to bind acrolein in urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Fibromyalgia

A

Chronic d/o with widespread MSS pain, fatigue neuropsychiatric disturbances in W 20-55 yo. Involves abnormal central processing of painful stimuli. Gradual incremental aerobic exercise can reduce pain. Normal acute phase reactants (CRP). Multiple tender points at characteristic locations. No joint or muscle inflammation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Polymyalgia rheumatica

A

Inflammatory d/o that affects patients >50yo, causes bilateral pain and morning stiffness in shoulders and hips, weight loss, fever, malaise, elevated ESR. Frequently associated with giant cell (temporal) arteritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Red rashes of childhood

A
  1. VZV
  2. Parvovirus B19
  3. Rubella virus
  4. Measles virus
  5. HHV6
  6. Streptococcus pyogenes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

VZV

A

Chicken pox. Pruritic, vesicular rash on face, trunk and extremities. Lesions in different stages of development.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Parvovirus B19

A

Erythema infectiosum. Malar rash with slapped cheek appearance (spares nasolabial folds. As rash fades, erythematous rash in reticular (lacelike) pattern appears in trunk and extremities. ***Aplastic crisis in sickle cell and immunocompromised patients.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Rubella

A

German measles. Togavirus. Maculopapular rash starting on head, progressing to trunk and extremities. Occipital & postauriricular lymphadenopathy. ***Congenital rubella syndrome.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Measles

A

Rubeola: Maculopapular rash starting on head that progresses to trunk and extremities. Rash preceded by cough, coryza, conjunctivitis, and koplik spots. ***Bronchopneumonia, encephalitits.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

HHV6

A

Roseola infantum: high fever for 3-5 days with rash once fever subsides. Macules & papules first on trunk, spread to extremities. Self limited.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Streptococcus pyogenes

A

Scarlet fever. Sandpaper-like rash (diffuse erythematous with small papules) that begins on neck, armpits, groin and then generalizes. A/w fever and sore throat. ***Rheumatic fever, glomerulonephritis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Drugs for BPH and HTN:

A

Doxazosin, prazosin, terazosin. Also beneficial for CAD, HF patients. A1B1 blockers. SE: first dose effect hypotension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Axonal reaction

A

Enlarged, rounded cells with peripherally located nuclei and dispersed finely granular nissle substance. Reflects incresed protein synthesis that facilitates axon repair.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How does botulinum intoxication present?

A

Descending paralysis that first manifests with cranial nerve abnl (diplopia, dysphagia, difficulty speaking). N/V/abd pain can occur in food-born botulinsm after consumption of contaminated, homemade canned foods. Incubation period is 12-36 hours. Pathophys: botonium toxin inhibits cholinergic nerves (nicotinic and muscarinic motor neurons), prevents binding and fusion of ACh-containing synaptic vesicles with plasma membrane, block relsease of ACh into NM synapse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Collagen synthesis

A

Procollagen is made in ER as a central helical structure flanked by globular extensions. Then transported through golgi and released into extracellular space where it’s converted into tropocollagen by procollagen peptidases (N and C terminal propeptides are removed) that remove globular portions of the molecule. The resulting tropocollagen monomers self-assemble into collagen fibrils that are then covalently crosslinked by lysyl oxidase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Kernicterus

A

Chorea, cerebral palsy, hearing loss, gaze abnl
Basal ganglia–caudate
Tx hyperbilirubinemia to prevent: phototherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Crigler-Najjar syndrome, type II tx

A

Phenobarbital induces liver enzyme synthesis (UDP-glucuronosyltransferase).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Wilson disease

A

AR. Defect in ATP7B enzyme: impaired excretion of copper into bile, impaired conversion of copper to ceruloplasmin –> low serum cerloplasmin.
Copper accumulates in liver, brain, cornea, kidneys, joints.
Sx: cirrhosis, Kayser-Fleischer ring, HCC risk, hemolytic anemia, basal ganglia degeneration, Parkinsonian sx, hepatic enceph, dementia, fanconi (PCT defect).
Tx: penicillamine (pennies–copper).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Hemochromatosis

A

Excess iron deposition.
Triad: cirrhosis, DM, skin pigmentation.
“Bronze DM.” CHF, testicular atrophy, increase risk of HCC.
AR (C282Y on HFE gene) results of transfusions.
Increased ferritin (storage iron). Increased total serum iron, decr total iron binding capacity, incr transferrin saturation.
Prussian blue stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

PBC vs PSC

A

PBC: +ANA, middle-aged woman, autoimmune
PSC: +pANCA, men > 40yo, a/w UC and cholangiocarcinoma, beads on string

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

S3 heart sound

A

Dilated cardiomyopathy
CHF
Mitral regurgitation
L to R shunt: VSD, ASD, PDA
Children (can be normal)
Pregnant woman (can be normal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

S4 heart sound

A

Late diastole, atrial kick
Stiffened LV wall
Hypertrophic cardiomyopathy
Aortic stenosis
Chronic HTN with LVH
Post-MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Which thalamic nuclei are the relay station for auditory sensation?

A

Medial geniculate nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Which thalamic nuclei are the relay station for visual sensation?

A

Lateral geniculate nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Which thalamic nuclei are the relay station for motor to the body?

A

Ventral lateral nucleus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Which thalamic nuclei are the relay station for facial sensation?

A

Ventral posteromedial nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Which thalamic nuclei are the relay station for body sensation?

A

Ventral posterolateral nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is PPAR-g? What is it used for?

A

Peroxisome proliferator-activated receptor gamma.
Nuclear receptors and TF found in adipose tissue. Plays role in adipocyte differentation. TZDs (thiazolidinediones) bind PPAR-g and improve insulin sensitivity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the acute phase cytokines?

A

IL1, IL6, IFNa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What agents are used in Parkinson’s?

A

BALSA: Bromocriptine (pramipexole), amantadine, levodopa (carbadopa), selegiline (entacapone), antimuscarinics (benztropine–helps with tremor only)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Where is Meissner’s plexus located?

A

Submucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Where is Auerbach’s plexus located? Also called myenteric plexus?

A

Outer layer of muscularis externa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is pulsus paradoxus and what are the causes?

A

SBP drops 10mmHg during inspiration.
Causes: overinflation of lungs: asthma, COPD, cardiac tamponade.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

FQ should not be given to which patients?

A

Children and pregnant women d/t risk of FQ induced joint toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the treatment for diabetes insipidus?

A
  1. Hydrochlorothiazide: help body concentrate urine
  2. Amiloride: closes sodium channel in collecting tubule, which is how lithium get into the cells.
  3. Indomethacin: reduce RBF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Which corticosteroid do you use for dangerous aldosterone deficiency?

A

Fludrocortisone: lots of mineralocorticoid activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the 4 tumors that secrete EPO?

A

Pheochromocytoma, RCC, hemangioblastoma, HCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What provides blood supply to thyroid and parathyroid glands?

A
  1. Superior thyroid artery: branch of external carotid artery
  2. Inferior thyroid artery: branch of thyrocervial trunk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Varus injury

A

Bowleg, adduction, LCL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Valgus injury

A

Knock nee, abduction, MCL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Medial epicondylitis

A

Golfer’s elbow, repetitive flexion, medial epicondyle pain. (Flexors come from medial side).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Lateral epicondylitis

A

Tennis elbow. Repetitive extension (backhand), lateral epicondyle pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Median nerve innervates which hand muscles?

A

1/2 LOAF: 1, 2 lumbricals, opponens pollicis, abductor pollicis brevis (recurrent branch), flexor pollicis brevis (superficial head)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Ulnar nerve innervates which hand muslces?

A

3/4 LOAF PAD: 3, 4 lumbricals, opponens digiti minimi, abductor digitis minimi, flexor digiti minimi brevis and deep head of flexor pollicis brevis, PAD, adductor policis, DAB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Lesions of which nerves cause foot drop?

A

PED = Peroneal Everts and Dorsiflexes. If injured – foot dropPED.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Lesion of which nerves prevent you from standing on tiptoes?

A

TIP = Tibial Inverts and Plantarflexes. If injured – can’t stand on TIPtoes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What does sciatic nerve innervate?

A

L4-S3: posterior thigh, splits into common peroneal and tibial nerves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What does pudendal nerve innervate?

A

S2-S4: innervates perineum. Can be blocked with local anesthetic during childbirth using ischial spine as landmark for injection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Type 1 muscle fibers

A

1 slow red ox: slow twitch, red fibers. More mitochondria and myoglobin concentration, sustained contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Type 2 muscle fibers

A

Fast twitch, white fibers. Less mitochondria and myoglobin concentration (more anaerobic glycolysis). Weight training results in hypertrophy of fast-twitch muscle fibers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are the following types of biological agents?
Rituximab, infliximab, certolizumab, imatinib, etanercept?

A

Rituximab: CD20 blocker for CD20+ non-Hodgkin’s lymphoma
Infliximab: TNF-a blocker for autoimmune diseases (Crohn’s, RA)
Certolizumab: pegylated humanized monoclonal Ab that targets TNF-a. Lacks Fc region (prevents complement and cell-mediated toxicity), treats autoimmune d/o associated with TNF-a
Imatinib: philadelphia chromosome + CML and kit-positive GI stromal tumors. Small-molecule tyrosine kinase receptor inhibitor.
Etanercept: TNFa inhibitor added to methotrexate for RA. Fusion protein linking soluble TNFa receptor to Fc part of human IgG1. DECOY.

86
Q

Rituximab

A

Rituximab: CD20 blocker for CD20+ non-Hodgkin’s lymphoma

87
Q

Infliximab

A

Infliximab: TNF-a blocker for autoimmune diseases (Crohn’s, RA)

88
Q

Certolizumab

A

Certolizumab: pegylated humanized monoclonal Ab that targets TNF-a. Lacks Fc region (prevents complement and cell-mediated toxicity), treats autoimmune d/o associated with TNF-a

89
Q

Imatinib

A

Imatinib: philadelphia chromosome + CML and kit-positive GI stromal tumors. Small-molecule tyrosine kinase receptor inhibitor.

90
Q

Etanercept

A

Etanercept: TNFa inhibitor added to methotrexate for RA. Fusion protein linking soluble TNFa receptor to Fc part of human IgG1. DECOY.

91
Q

cAMP pathway

A

FLAT ChAMP
FSH
LH
ACTH
TSH
CRH
hCG
ADH (V2 receptor)
MSH
PTH
Also: calcitonin, GHRH, glucagon

92
Q

cGMP pathway

A

Think vasodilators
ANP, BNP, NO (EDRF)

93
Q

IP3 pathway

A

GOAT HAG
GnRH
Oxytocin
ADH (V1 receptor)
TRH
Histamine (H1 receptor)
Angiotensin II
Gastrin

94
Q

Intracellular receptor pathway

A

VETTT CAP
Vitamin D
Estrogen
Testosterone
T3/T4
Cortisol
Aldosterone
Progesterone

95
Q

Intrinsic tyrosine kinase pathway

A

MAP kinase pathway, think growth factors
Insulin, IGF-1, FGF, PDGF, EGF

96
Q

Recetor-associated tyrosine kinase pathway

A

JAK/STAT pathway, think acidophils and cytokines
PIGGlET
Prolactin
Immunomodulators (cytokines IL2, IL6, IFN)
GH
G-CSF
Erythropoietin
Thrombopoietin

97
Q

Key features of osteoarthritis

A

Subchondral cysts, sclerosis, osteophytes (spurs), eburnation, synovitis
Herberden (DIP)
Bouchard (PIP)
No MCP involvement
Knee cartilage loss begins medially –> bowlegged
Noninflammatory, no systemc sx
Tx: acetaminophen, NSAIDs, intraarticular glucocoriticoids

98
Q

Key features of rheumatoid arthritis

A

Autoimmmune, inflammatory destruction of synovial joints
Pannus (inflammatory granulation tissue = BV, fibroblasts, myofibroblasts) in MCP and PIP
SQ rheumatoid nodules (fibrinoid necrosis)
Ulnar deviation
Subluxation
Swan neck and boutonniere deformities
No DIP
Baker cyst, vasculitides, interstitial lung fibrosis.
80% have rheumatoid factor (anti-IgG ab), anti-cyclic citrullinated peptide b (more specific)
HLA-DR4
Tx: NSAIDs, glucocorticoids, disease-modifying agents (methotrexate, sulfasalazine), biologics (TNF-a inhibitors)

99
Q

HLA Subtypes

A

A3: Hemochormatosis
B27: PAIR (seronegative arthropathies) – Psoriatic arthritis, Ankylosing spondylitis, arthritis of IBD, Reactive arthritis (Reiter)
DQ2/DQ8: celiac disease
DR2: MS, hay fever, SLE, Goodpasture syndrome
DR3: DMTI, SLE, Graves, Hashimoto
DR4: Rheumatoid arthritis (4 walls in rheum “room”), DMTI
DR5: pernicious anemia–>VB12 deficiency, Hashimoto

100
Q

Positive (upregulated) acute-phase reactants

A

CRP: opsonin, fixes complement and faciliates phagocytosis. Measures ongoing inflammation.
Ferritin: binds and sequesters iron to inhibit microbial iron scavenging.
Fibrinogen: coagulation factor, promotes endothelial repair, correlates with ESR.
Hepcidin: prevents release of iron bound by ferritin –> anemia of chronic disease.
Serum amyloid A: prolonged elevation –> amyloidosis.

101
Q

Negative (downregulated) acute-phase reactants

A

Albumin: reduction conserves Aas for positive reactants.
Transferrin: internalized by MO to sequester iron.

102
Q

ACEI are contraindicated in patients with a deficiency of what?

A

C1 esterase inhibitor deficiency. Causes heriditary angioedema. Increases bradykinin.

103
Q

ACEI are CI in patients with:

A
  1. Bilateral renal artery stenosis: ACEI decrease GFR, leading to renal failure
  2. C1 esterase inhibitor deficiency (hereditary angioedema): icnreased complement activity–>incr bradykinin–>mets by ACE
  3. Pregnancy: fetal renal damage
104
Q

Exposure to which organisms require passive immunity?

A

To Be Healed Very Rapidly
Tetanus toxin, Botulinum toxin, HBV, Varicella, or Rabies
Passive immunity = pre-formed antibodies

105
Q

What are the live attenuated vaccines?

A

Measles, mumps, rubella (MMR), polio (Sabin), influenza (intranasal), varicella, yellow fever
*may revert to virulent form

106
Q

What are the killed vaccines?

A

RIP Always
Rabies, Influenza (injection), Polio (Salk), hepatitis A

107
Q

What are the catalase + organisms?

A

Need PLACESS
Nocardia, Pseudomonas, Listeria, Aspergillus, Candida, E. coli, S. aureus, Serratia

108
Q

What phase of meiosis is a primary oocyte arrested in until before ovulation? What is it arrested in until fertilization?

A

Arrested until ovulation: primary oocyte in prophase of meiosis I
Arrested until fertilization: secondary oocyte in metaphase of meiosis II

109
Q

What drugs are used for pulmonary HTN?

A
  1. Endothelin receptor antagonist: bosentan. Decr pulmonary vascuar resistance.
  2. PDE-5 inhibitors: sildenafil. Inhibit cGMP PDE5, prolong vasodilatory effect of NO.
  3. Prostacyclin analogs: epoprostenol, iloprost. PGI2 with direct vasodilatory effects on pulmonary and systemic arterial vascular beds. Inhibit platelet aggregation. SE = flushing and jaw pain.
110
Q

Cytoskeleton:
Actin
Myosin
Tubulin
Kinesin
Dynein

A

Actin: monomeric units that comprise cytoskeletal structural microfilaments
Myosin: microfilament proteins that are directed toward the + end of filament
Tubulin: monomeric units that comprise MT (necessary for movement of cargo through cell)
Kinesin: motor proteins that move cargo toward the + end of the MT (anterograde)
Dynein: motor protiens that move cargo toward the - end of the MT (retrograde)

111
Q

Pemphigus vulgaris

A

Lesions begin in oral mucosa
Acantholysis with intradermal blisters seen
Nikolsky sign +
IgG abs direct against desmoglein (cell-cell adhesion)

112
Q

Cytotrophoblast

A

Makes Cells. Inner layer of chorionic villi. Stem cells.

113
Q

Syncytiotrophoblast

A

Outer layer of chorionic villi, secretes hCG–similar to LH, stimulates corpus luteum to secrete progesterone during first trimester.
***Lacks MHC-I expression: decrease chance of attack by maternal immune system.

114
Q

Pathway of sperm during ejaculation

A

SEVEN UP: seminiferous tubules, epididymis, vas deferens, ejaculatory ducts, (nothing), urethra, penis

115
Q

Bowen disease

A

Leukoplakia in penile shaft and scrotum. >35yo, HPV 16, 18.

116
Q

Erythroplasia of Queyrat

A

Cancer of glans and prepuce. Presents as erythroplakia. HPV16.

117
Q

Bowenoid papulosis

A

Multiple pigmented red/brown papules on external genitalia. Carcinoma in situ of unclear malignant potential.

118
Q

What is Anserine bursitis?

A

Pes anserinus bursitis–medial aspect of knee. Results from overuse in atheletes or from chronic trauma in patients with heavy body habitus.

119
Q

Which muscles contribute to the pes anserinus?

A

Sergeant FOT: Sartorius, Gracillis, semiTeniosis (medial to lateral), Femoral nerve, Obturator nerve, Tibial nerve

120
Q

NE is made in _____, increased in _____, decreased in _____.

A

Locus ceruleus (pons)–stress and panic
Increased in anxiety
Decreased in depression

121
Q

DA is made in _____, increased in _____, decreased in _____.

A

Ventra tegmentum and substatia nigra pars compacta (midbrain)
Increased in Huntinton disease
Decreased in Parkinson and depression

122
Q

5-HT is made in _____, increased in _____, decreased in _____.

A

Raphe nuclei (pons, medulla, midbrain)
Increased in nothing
Decreased in anxiety and depression

123
Q

ACh is made in _____, increased in _____, decreased in _____.

A

Basal nucleus of Meynert
Increased in Parkinson disease
Decreased in Alzheimer and Huntington

124
Q

GABA is made in _____, increased in _____, decreased in _____.

A

Nucleus accumbens–reward center, pleasure, addiction, fear
Increased in nothing
Decreased in anxiety and Huntington
***Main inhibitory neuron from glutamate, needs B6

125
Q

What are some RFs and TXs for pseudotumor cerebri?

A

RF: woman of childbearing age, vitamin A excess, danazol
Treatment: weight loss, acetazolamide, topiramate (GABA release, antisiezure), invasive procedures for refractory cases

126
Q

Which muscles close the jaw? Which opens?

A

Close jaw: Masseter, teMporalis, Medial pterygoid (M’s Munch)
Open jaw: lateral pterygoid (Lateral Lowers)

127
Q

How does retinal detachment present?

A

Breaks are most common in patients with high myopia and are often preceded by posterior vitreous detachment (flashes and floaters) and eventual monocular loss of vision like a curtain drawn down. EMERGENCY.

128
Q

Miosis pathway

A

1st neuron: Edinger-Westphal nucleus to ciliary ganglion via CN III
2nd neuron: short ciliary nerves to pupillary sphincter muscles

129
Q

Mydriasis pathway

A

1st neuron: hypothalamus to ciliospinal center of Budge
2nd neuron: exit at T1 to superior cervical ganglion (travels along cervical sympathetic chain near lung apex, subclavian vessels)
3rd neuron: plexus along internal carotid, thorugh cavernous sinus, enters orbit as long ciliary nerve to pupillary dilator muscles. Sympathetic fibers also innervate smooth muscle of eyelids (minor retractors) and sweat glands of forehead and face.

130
Q

How do cholinergic agonists affect glaucoma?

A

Cholinergic agonists (pilocarpine and carbachol) cause miosis by promoting contraction of the sphincter of iris. This causes the anterior chamber angle to become wider, making the trabecular meshwork more accessible to outflow of the aqueous humor.

131
Q

How do a-agonists treat glaucoma (which kind)?

A

a-agonists (epinephrine, brimonidine) are used for open angle only.
Decrease aqueous humor synthesis.
***Causes mydriasis (do not use in closed-angle). This would lead to further closing of trabecular meshwork (via narrowing of the uveoscleral outflow tract) –> decreased flow of aqueous humor.

132
Q

Pure motor hemiparesis

A

Posterior limb of the internal capsule or basal pons

133
Q

Pure sensory stroke

A

VPL or VPM thalamus

134
Q

Ataxis-hemiplegia syndrome

A

Posterior limb of the internal capsule or basal pons

135
Q

Dysarthria-clumsy hand syndrome

A

Genu of the internal capsule or basal pons

136
Q

Biofilm-producing organisms

A

Staphylococcus epidermidis (catheter, prosthetics)
Streptococcus mutans & sanguinis (dental plaques)
Pseudomonas aeruginosa (CF pneumonia, contact lenses)
Viridans group streptococci (endocarditis)
Nontypable H. influenza (otitis media)

137
Q

Local anesthetics–Esters

A

Procaine, cocaine, tetracaine

138
Q

Local anesthetics–Amides

A

Lidocaine, mepivacain, bupivacaine (all have 2 I’s)

139
Q

Order of nerve blockade (local anesthetic)

A

Small-diameter fibers > large
Myelinated fibers > unmyelinated fibers

140
Q

Order of nerve sensation loss (local anesthetic)

A

Pain, temp, touch, pressure

141
Q

Depolarizing NM blocking drugs

A

Succinylcholine: strong Ach receptor agonist, produces sustained depolarization and prevents muscle contraction.
Reversal of blockage: Phase I–prolonged depolarization/NO ANTIDOTE. Block potentiated by cholinesterase inhibitors. Phase II–repolarized but blocked/ACh receptors are available, but desensitized. Antidote: cholinesterase inhibitors.
Complications: hypercalcemia, hyperkalemia, malignant hyperthermia

142
Q

Nondepolarizing NM blocking drugs

A

Tubocurarine, atracurium, mivacurium, pancuronium: all are competitive antagonists and compete with ACh for receptors.
Reversal of blockage: neostigmeine (must be given with atropine to prevent muscarinic effects like bradycardia), edrophonium, other cholinesterase inhibitors.

143
Q

Therapeutic supplemental O2 for neonatal respiratory distress syndrome can lead to what?

A

RIB: retinopathy of prematurity, intraventricular hemorrhage, and bronchopulmonary dysplasia

144
Q

MCC of lobar pneumonia

A

S. pneumo: CAP
Klebsiella: aspiration, nursing home
Legionella

145
Q

MCC of bronchopneumonia

A

Staph aureus: secondary, abscess, empyema
H. influenzae: superimposed on COPD
Pseudomonas: cystic fibrosis
Moraxella catarrhalis: CAP + superimposed on COPD
Legionella: CAP, on COPD, water source, intracellular, silver stain

146
Q

MCC of interestitial (atypical) pneumonia

A

Mycoplasma: military or dorm, IgM autoimmune hemolytic anemia, erythema multiforme, no cell wall
Chlamydia: young adults
RSV: infants
CMV: post-transplant immunosuppressive therapy
Influenza virus: immunocompromised, elderly, lung dz, increased secondary bacterial
Coxiella: Q fever, farmer and vets, ricketssial but no vector

147
Q

Apiration pneumonia

A

R lower lobe abscess
Alcoholic and comatose
Anaerobes: bacteroides, fusobacterium, peptostreptococcus
S. aureus
Tx: clindamycin

148
Q

MI myocyte progression

A

0-4: minimal
4-12: early coagulation necrosis, edema, hemorrhage, wavy fibers
12-24: coagulation necrosis and marginal contraction band necrosis
1-5 days: coagulation necorsis and neutrophilic infiltrate
5-10 days: macrophage phagocytosis of dead cells
10-14 days: granulation tissue and neovascularization
2 weeks to 2 months: collagement deposition/scar formation

149
Q

Conditions with increased pulse pressure and decreased pulse pressure

A

Increased PP: hyperthyroidism, aortic regurgitation, aortic stifening (isolated systolic HTN in elderly), OSA (increased sympathetic tone), exercise (transient).

Decreased PP: aortic stenosis, cardiogenic shock, cardiac tamponade, advanced heart failure (HF).

150
Q

Conditions that increase myocardial O2 demand

A

Increased: contractility, afterload (proportional to arterial pressure), HR, diameter of ventricle (wall tension)

***Wall tension = (Pressure * radius)/(2 * thickness)

151
Q

VIPoma

A

WDHA syndrome: watery diarrhea, hypokalemia, achlorhydria

152
Q

Somatostatinoma

A

d-cell, a/w DM, steatorrhea, cholelithiasis, hypochlorhydria
Blocks insulin, gastrin, secretin, CCK, and GI motility

153
Q

Advance directives

A
  1. Living will: specifies end of life wishes–regarding intubation, cardiopulmonary resuscitation, enteral feeding, life-prolonging interventions.
  2. Health care proxy: individual to make health care decisions, decisions must be made in accordance with patient’s wishes outlined in will.
154
Q

What are 3 organisms that can undergo transformation?

A

SHiN: S. pneumo, H. influenzae B, Neisserina

155
Q

What are 5 bacterial toxins that are encoded in a lysogenic phage?

A

ShigA-like toxin
Botulinum toxin (certain strains)
Cholera toxin
Diphtheria toxin
Erythrogenic toxin of S. pyogenes

156
Q

Which drugs have 0-order elimination?

A

PEA (round, 0): phenytoin, ethanol, aspirin

157
Q

How do you treat salicylate OD?
How do you treat amphetamine OD?

A
  1. Acidic drug OD (salicylate): NaHCO3 to trap acidic drug in basic urine
  2. Basic drug OD (amphetamines): Na4Cl to trap basic drug in acidic urine
158
Q

Fanconi syndrome

A

Generalized resorptive defect in PCT. Increased excretion of all AAs, glucose, HCO3-, PO43-. Results in metabolic acidosis.
Causes: hereditary defects (Wilson, tyrosinemia, glycogen storage dz), ischemia, MM, nephrotoxins/drugs (expired tetracycline, tenofovir), lead poisoning.

159
Q

Relative concentrations along PCT

A

PAH > Creatinine > Inulin&raquo_space; Urea > Cl- > K+ > Na+ > osmolarity > Pi&raquo_space; HCO3-&raquo_space; AA > Glucose

160
Q

Potassium shifts

A
  1. Hyperkalemia (shifts K+ out of cell): DO LABS. Digitalis (blocks Na+/K+ ATPase), hyperOsmolarity, Lysis of cells (crush injury, rhabdomyolysis, cancer), Acidosis, B-blocker, high blood Sugar (low insulin). Also K+sparing diuretics, ACEI, digoxin.
  2. Hypokalemia (shifts K+ into cell): hypo-osmolarity, alkalosis, b-adrenergic agonist (increased Na+/K+ ATPase), insulin (increased Na+/K+ ATPase), INsulin shifts K+ INto cells. Also–Loop diuretics, thiazides.
161
Q

Renal tubular acidosis–Type 1

A

Type I/Distal: urine pH > 5.5. Defect in a-intercalated cells to secrete H+ –> no new bicarb generated –> metabolic acidosis. Hypokalemia, incr risk for CaPhos kidney stones (incr urine pH and incr bone turnover).
Causes: amphotericin B, analgesic nephropathy, congenital anomalies (obstruction of UT).

162
Q

Renal tubular acidosis–Type 2

A

Type 2/Proximal: urine pH

163
Q

Renal tubular acidosis–Type 4

A

Type 4/Hyperkalemic: urine pH hyperkalemia –> decr NH3 synthesis in PCT –> decr NH4 excretion.
Causes: decr aldosterone production (diabetic hyporeninism, ACEI, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency), or aldosterone resistance (K+-sparing diuretics, nephropathy d/t obsturction, TMP/SMX).

164
Q

Acute Interstitial Nephritis

A

AKA Drug-induced interstitial nephritis
Classic presentation: fever, rash, eosinophilia, azotemia
MCC: NSAIDs, PCN/cephalosporins, sulfonamides (TMP-SMX, furosemide), ciprofloxacin, cimetidine, allopurinols, PPIs, indinavir, mesalamine.

165
Q

Diffuse coritcal necrosis

A

Multiorgan failure, ARDS, DIC
Associated with obstetric catastrophes (abruptio placentae), septic shock

166
Q

Acute tubular necrosis

A

Findings: granular casts (necrotic epithelial cells).
Inciting phase. Maintenence phase: oliguric, 1-3 weeks, risk of hyperkalemia, metabolic acidosis, uremia. Recovery phase: risk of hypokalemia during re-epithelization of tubules.
Drugs/toxins: aminoglycosides, cephalosporins, polymyxins, radiograph contrast dye (prevent with fluids, NaHCO3)
Rhabdomyolysis/myoglobinuria (muscle breakdown from seizure d/o, cocaine, or crush injury)–4+ blood in urine, no RBC on urine cell count, renal failure, elevated CPK.

167
Q

Renal papillary necrosis

A

SAAD papa with papillary necrosis: sickle cell disease or trait, acute pyelonephritis, analgesics (NSAIDs), Diabetes mellitus
Sloughing of necrotic renal papillae –> gross hematuria and proteinuria. Can be triggered by recent infxn or immune stimulus.

168
Q

Consequences of renal failure

A

MADHUNGER
Metabolic Acidosis
Dyslipidemia (increased TG)
Hyperkalemia
Uremia: increased BUN–N/anorexia, pericarditis, asterixis, encephalopathy, platelet dysfunction
Na+/H2O retention (HF, pulmonary edema, hypertension)
Growth retardation and developmental delay
Erythropoietin failure (anemia)
Renal osteodystrophy

169
Q

Wilms tumor

A

Nephroblastoma. MC ages 2-4. Embryonic glomerular structures.
Loss of function mutations of WT1/WT2 (tumor suppressors) on chromosome 11.
Beckwith-Widemann: Wilms tumor, macroglossia, organomegaly, hemihypertrophy
WAGR complex: Wilms tumor, Aniridia, GU malformation, mental Retardation

170
Q

Renal oncocytocytoma

A

Benign epithelial cell tumor of collecting duct cells
Large eosinophilic cells with abundant mitochondria WITHOUT perinuclear clearing (vs RCC).

171
Q

RCC

A

PCT cell tumor–polygonal clear cells with accumulated lipids and carbs. Hematuria, palpable mass, secondary polycythemia, flank pain, fever, weightloss.
Invades renal vein then IVC and spreads, mets to lung and bone.
A/w Von Hippel-Lindau (chr 3)
Paraneoplastic: EPO, ACTH, PTHrP

172
Q

Acute poststreptococcal glomerulonephritis

A

IF: granular lumpy-bumpy, IgG, IgM, C3 deposition along GBM and mesangium
EM: subepithelial immune complex (IC) humps
2 weeks after group A strep of pharynx or skin
Type 3 HSN
Peripheral and periorbital edema, cola-colored urine, HTN
Anti-Dnase B titers, decr complement

173
Q

RPGN

A

LM and IF: crescent moon shape–fibrin and plasma protein (C3b) with glomerular parietal cells, monocytes, MO.
*Goodpasture: type 2 HSN, anti-GBM and alveolar basement – linear IF
*Granulomatosis with polyangiitis (Wegener) – c-ANCA (PR3)
*Microscopic polyangiitis – p-ANCA (MPO)
Tx: emergent plasmapheresis

174
Q

DPGN (diffuse proliferative)

A

Due to SLE or membranoproliferative glomerulonephritis
LM: wire looping
EM: subendothelial, sometimes intramembranous IgG-based Ics with C3 deposition
IF: granular
*MCC of death in SLE (wire lupus)

175
Q

IgA nephropathy (Berger)

A

LM: mesangial proliferation
EM: mesangial IC deposits
IF: IgA-based IC deposits in mesangium
Renal pathology of Henoch-Schonlein purpura
*Often presents with renal insufficiency or acute gastroenteritis. Episodic hematuria with RBC casts.

176
Q

Alport syndrome

A

Mutation in type IV collagen – thinning and splitting of glomerular BM. X-linked!
*Can’t see, can’t pee, can’t hear a buzzing bee.
*Eye problems (retinopathy, lens dislocation), glomerulonephritis, sensorineural deafness

177
Q

MPGN (membranoproliferative)

A

Type I: subendothelial IC deposits with granular IF. Tram-track on PAS from GBM splitting caused by mesangial ingrowth. Hepatitis B/C!!!
Type II: intramembranous IC deposits, dense deposits. C3 neprhitic factor (stabilizes C3 convertase, decr serum C3)!!!

178
Q

Focal segmental glomerulosclerosis

A

LM: segmental sclerosis and hyalinosis
IF: nonspecific for focal deposits of IgM, C3, C1
EM: effacement of foot process (like minimal change)
MCC of nephrotic syndrome in AA and Hispanics.
HIV, sickle cell, heroin abuse, obsesity, interferon tx, CKD.

179
Q

Minimal change disease (lipoid nephrosis)

A

LM: normal glomeruli
IF: nothing
EM: effacement (fusion) of foot processes.
MCC of nephrotic syndrome in children. Often idiopathic and triggered by recent infection, immunization, immune stimulus, atopic dermatitis.

180
Q

Membranous nephropathy

A

LM: diffuse capillary and GMB thickening
IF: granular as a result of IC deposition. Nephrotic presentation of SLE.
EM: spike and dome with subepithelial deposits
MCC of nephrotic syndrome in Caucasians. Can be secondary to drugs (NSAIDs, PCN), infxn (HBV, HCV), SLE, tumors.

181
Q

Amyloidosis

A

LM: Congo red stain shows apple-green birefringence under polarized light.
A/w chronic conditions (MM, TB, rheum arthritis)

182
Q

Diabetic glomerulonephropathy

A

LM: mesangial expansion, GMB thickening, eosinophilic nodular glomerulosclerosis (Kimmelsiel-Wilson)
Nonenzymatic glycosylation of GBM leads to increased permeability, thickening.
Nonenzymatic glycosylation of efferent arterioles –> increased GFR –> mesangial expansion.

183
Q

Bartter syndrome

A

Thick ascending loop–Na/K/Cl cotransporter.
Hypokalemia, metabolic alkalosis, hypercalciuria.

184
Q

Gitelman syndrome

A

NaCl in DCT–mimics thiazide diuretic.
Less severe than Bartter.
Hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria.
Muscle weakness, tetany, fatigue (hypoK and Mg)

185
Q

Liddle syndrome

A

Gain of function mutation: increased Na reabs in CT (increased ENAC).
Autosomal dominant.
HTN, hypokalemia, metabolic alkalosis, decreased aldosterone.
Tx: amiloride (block Enac)

186
Q

Syndrome of apparent mineralocorticoid excess = AME

A

Deficiency of 11b-hydroxysteroid dehydrogenase. Normally converts cortisol into cortisone before cortisol can act on mineralocoritcoid receptors.
Excess coritsol –> HTN, hypokalemia, metabolic alkaosis. Low aldosterone.
Glycyrrhetic acid (licorice).

187
Q

Chlorpropamide, tolbutamide

A

First gen sulfonylureas. Close K+ channel in b-cell membrane –> insulin release via calcium influx. SE: disulfiram effects.

188
Q

Glimepiride, glipizide, glyburide

A

2nd gen sulfonylureas. SE: hypoglycemia

189
Q

Pioglitazone, rosiglitazone

A

Glitazones/thiazolidinedions. Increase insulin sensitivity in peripheral tissue. Binds to PPAR-g nuclear transcription regulator. SE: weight gain, edema, hepatotoxicity, HF, increase risk of fractures.

190
Q

Exenatide, liraglutide

A

GLP-1 analogs. Increase insulin, decrease glucagon release. SE: N/V, pancreatitis.

191
Q

Linagliptin, saxagliptin, sitagliptin

A

DPP-4 inhibitors. Increase insulin, decrease glucagon release. Mild urinary or respiratory infections.

192
Q

Pramlintide

A

Amylin analogs. Decrease gastric emptying, decrease glucagon. Type 1 and type 2 DM. SE: hypoglycemia, N/D.

193
Q

Canagliflozin

A

SGLT-2 inhibitors. Block reabs of glucose in PCT. Type 2 DM. SE: Glucosuria, UTIs, vaginal yeast infections.

194
Q

Acarbose, miglitol

A

a-glucosidase inhibitors. Inhibit intestinal brush-border a-glucosidases. Delayed carb hydrolysis and glucose abs, decreases post prandial hyperglycemia. SE: GI.

195
Q

Nimodipine

A

Subarachnoid hemorrhage (prevents cerebral vasospasm)

196
Q

Clevidipine

A

HTN urgency or emergency

197
Q

Nitroprusside

A

Releases NO, which generated cGMP in smooth muscle of arteries and veins. Reduces preload and afterload.
Use: HTN emergency, given by IV infusion
SE: rebound HTN, cyanide toxicity (co-admin with nitrates and thiosulfate to decr toxicity).

198
Q

Refeeding syndrome and hypophosphatemia

A

Serum phosphate

199
Q

Narcolepsy

A

Decreased hypocretin (orexin) production in lateral hypothalamus

200
Q

FAB GUT
Galactokinase def, classic galactosemia

A

Fructose is to Aldolase B as Galactose is to UridylTransferase

201
Q

Target cell–HALT

A

HALT said the hunter to his target
HbC, Asplenia, Liver disease, Thalassemia

202
Q

Porphobilinogen deamniase deficiency

A

Acute intermittent porphyria
5 P’s: Painful abd, Port wine-colored urine, Polyneuropathy, Psychological disturbances, Precipitated by drugs (cytochrom P450 inducers), alcohol, starvation.
Tx: glucose and heme (inhibit ALA synthase)

203
Q

Uroporphyrinogen decarboxylase deficiency

A

Porphyria cutanea tarda
Tea-colored urine–uroporphyrin build up
Blistering cutaneous photosensitivity, MC!!
Hypertrichosis, facial hyperpigmentation, hepatitic C, alcoholism, incr LFTs

204
Q

Lead poisoning

A

Ferrochelatase and ALA dehydratase
Adults: HA, memory loss, demyelination, foot/wrist drop
Kids: mental deterioation
Colicky abd pain – renal failure
Tx: EDTA or succimer. Severe–dimercaperol and succimer

205
Q

Potentially Really High Hematocrit

A

Pheohromocytoma, RCC, HCC, Hemangioblastoma

206
Q

Orotic aciduria

A

Deficiency of UMP synthase (pyrimidine synthesis), can’t make UMP
Orotic acid in urine, Megaloblastic anemia
Presentation: FTT, developmental delay, megaloblastic refractory to B12/folate.
No hyperammonemia (vs. ornithine transcarbamylase def)
Tx: uridine monophosphate to bypass mutated enzymme.

207
Q

Fanconi anemia

A

DNA repair defect–non-homologous end joining
Causes aplastic anemia

208
Q

Pyruvate kinase deficiency

A

Glycolytic enzyme deficiency, can’t make ATP, RBC swelling and hemolysis.
Survive on reticulocytes (still have organelles and can do oxidative phosphorylation, increase 2,3BPG (easier release of O2)

209
Q

Waldenstrom macroglobulinemia

A

M spike = IgM –> hyperviscosity syndrome (blurred vision, Raynaud), no CRAB.

210
Q

Pseudo Pelger Huet anomaly

A

Neutrophils with bilobed nuclei. Seen after chemotherapy.

211
Q

Hairy cell leukemia tx

A

Cladribine–2CDA (adenosine deaminase inhibitor–adenosine accumulates, toxic to B cells), pentostatin

212
Q

Nerve courses

A

Median: between humeral and ulner heads of pronator teres muscle, runs between flexor digitorum superficialis and the flexor digitorum profundus within carpal tunnel.

Musculocutaneous: between biceps and coracobrachialis. Injury: bicep and brachilais paralysis.

Ulnar: between olecranon and medial epicondyle of humers (funnybone). Also between flexor carpi ulnaris and flexor digitorum profundus in forearm. Injury: claw hand due to loss of intrinsic muscles of hand.

Radial: through supinator muscle near head of radius. Injury: wrist drop.

Boards (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions