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(DIT) Rapid Fire + 4/5 Stars > 4 and 5 star items > Flashcards

4 and 5 star items Flashcards

1
Q

Neural Crest Derivatives

A

MAGIC COPS

Melanocytes
Aortic pulmonary septum
Ganglia - autonomic, dorsal root, enteric - Peripheral nervous system
Iris stroma
Chromatin cells (adrenal medulla)
Cranial nerves
Odontoblasts/Ossicles
Parafollicular (C) cells
Sclerae
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2
Q

Whiteboard derivatives of arachidonic acid and pharmacologic inhibitors

A

Page 15 DIT workbook

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3
Q

Label circle of willis worksheet

A

answers page 38 DIT workbook

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4
Q

Gertsmann syndrome

A

lesion of DOMINANT angular gyrus of parietal lobe

agraphia - can’t write
acalculia - can’t do math
Right -left disorientation
Finger agnosia - can’t distinguish fingers

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5
Q

Hemispatial neglect syndrome

A

lesion to NONDOMINANT angular gyrus of parietal lobe

Neglect body or surroundings contralateral to lesion

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6
Q

Symptoms of lateral medullary syndrome (Wallenberg Syndrome)?

A

Loss of pain and temp over contralateral body - spinothalamic tract

Loss of pain/temp over ipsilateral face - spinal trigeminal nucleus damage

Hoarseness, difficulty swallowing, loss of gag reflex - nucleus ambiguus, CN IX and X damage

Ipsilateral Horner syndrome - descending sympathetic tract

Vertigo, nystagmus, N/V - vestibular nuclei damage!

Ipsilateral cerebellar defects - ataxia, past pointing - inferior cerebellar peduncle damage - spinocerebellar tract

Assoc w/ PICA occlusion

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7
Q

Medial medullary syndrome

A

contralateral spastic hemiparesis - pyramid/corticospinal tract damage

Contralateral tactile and kinesthetic defects - medial lemniscus damage

Tongue deviates toward side of lesion - hypoglossal nucleus/nerve damage

Pain and temp preserved

Assoc w/ anterior spinal a. occlusion

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8
Q

Lateral inferior pontine syndrome

A

ipsilateral facial nerve paralysis - facial nucleus and fiber damage

Ipsilateral limb and gait ataxia - damage to middle cerebellar peduncle

Ipsilateral loss of pain and temp from face - spinal trigeminal nucleus and nerve damage

contralateral loss of pain/temp - damage to spinothalamic tract

Ipsilateral Horner Syndrome - damage to descending sympathetic tract

No contralateral body paralysis or loss of light touch/vibratory/proprioceptive sensation

Assoc w/ AICA occlusion

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9
Q

Medial pontine syndrome

A

Contralateral spastic hemiparesis - corticospinal tract

Contralateral loss of light touch/vibratory/proprioceptive sensation - ML damage

Ipsilateral INO - MLF damage

Gaze away from side of lesion - PPRF

Ipsilateral paralysis of LR m. - damage to abducens nucleus

Pain and temp preserved

Basilar A - median and paramedian branches occluded

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10
Q

Weber Syndrome

A

occlusion of paramedian branches of PCA

Cerebral peduncle lesion:

  • dysphagia, dysphonia, dysarthria - corticobulbar tract
  • Contralateral spastic hemiparesis - corticospinal tract

Oculomotor n. palsy –> ipsilateral ptosis, pupillary dilation, lateral strabismus (down and out)

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11
Q

Tension Headache

A

Constant, non-throbbing pain - hours to 7 days

Frontal or occipital regions (b/l) or as band around head

No associated sx like photo/phono-phobia, auras, n/v, focal neurologic change

Tx: NSAIDs, Acetaminophen

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12
Q

Migraine Headache

A

At least 5 attacks

Lasts 4-72 hours (2-48 in kids)

At least 2 of the following: u/l location, throbbing, pulsating quality, moderate to severe intensity (inhibits/prohibits daily activities), aggravated by routine physical activity

At least one of the following: N/V, photo- and/or phono-phobia

Tx: Triptans (sumatriptan, rizatriptan, zolmitriptan): serotonin agonists –> vasoconstriction, modulates neurotransmission in CN V
CONTRAINDICATED in CAD, prinzmedal angina, pregnancy

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13
Q

Cluster Headache

A

Strictly unilateral
Severe piercing/boring pain in periorbital/retroorbital region
does not throb like migraine, no aura
15 min - 3 hours, daily at same time, continues for 4-8 weeks

May be associated w/:
Partial Horner syndrome - ptosis, miosis
Ipsilateral eye redness, tearing, rhinorrhea, nasal congestion

Tx: 100% O2 in nonrebreather mask for 15 minutes

Can also use triptans, NSAIDs, Acetaminophen

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14
Q

Alzheimer Disease

A

Tau neurofibrillary tangles
Senile plaques - Abeta extracellularly

Early onset: Presenilin 1,-2; Amyloid precursor protein (APP) on Chr 21 (why Downs get it in 40s)

late onset: ApoE4 –> beta sheets

Tx: Slow down progression

  • AChEI: Donepizil, Galantium, Rivastigmine
  • NMDA receptor antagonist: Memantine -decreases excitotoxicity
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15
Q

Vascular Dementia

A

White matter ischemic changes on MRI

d/t atherosclerosis

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16
Q

Dementia w/ Lewy Bodies

A

alpha synuclein protein
Parkinsonian features
Visual hallucinations
Syncopal episodes = falls

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17
Q

Frontotemporal dementia

A

aka Picks

Tau on silver stain - pick bodies
atrophy of frontal/temporal lobes

Dementia + behavior/personality changes - more crass

Demential + progressive aphasia - can’t understand what is being said to them

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18
Q

Creutzfeldt-Jakob Disease

A

RAPIDLY progressing demential - weeks-months
personality change
muscle spasms
myoclonus

PrpSc - beta pleated sheets –> spongiform encephalopathy

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19
Q

Work up for Alzheimers

A

RPR - r/o neurosyphilis
HIV
B12 levels
If dysarthria and liver dz present think Wilsons
TSH - r/o hypothyroidism
MRI to look for normal pressure hydrocephalus, vascular dementia
Screen for depression in elderly - will recognize problem

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20
Q

Causes of Delirium

A

UTI, infections, fevers

Drugs: bentos, anticholinergic side effects, withdrawal or drug abuse

hypoxemia
electrolyte imbalance

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21
Q

Delirium vs dementia: Onset, Daily course, consciousness, thought, psychotic, prognosis

A

Onset: Delirium acute (hours to days), Demential gradual (mo-yrs)

Daily course: Delirium fluctuates, dementia consistent

Level of consciousness: Delirium decreased arousal, demential normal

Thought production: delirium disorganized thinking, flight of ideas; dementia impoverished

Psychotic features: delirium visual hallucinations, delusions; dementia - minimal

Prognosis: delirium - reversible, dementia - irreversible

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22
Q

Location/function of Muscarinic receptors

A

M1: enteric NS
M2: heart - decreases contractility, lowers HR via SA node
M3: increase bladder contraction, increase gut peristalsis, lacrimation, mitosis, bronchoconstriction

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23
Q

Epi/NE receptor functions

A

a1 - vascular sm.m. constriction - vasoconstriction
a2 - inhibit NE release
b1 - increase HR, contractility
b2 - vasodilation, bronchodilation

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24
Q

Dopamine receptor function/location

A

D1 - relax renal vascular sm.m.

D2 - brain

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25
Q

Histamine receptor function

A

H1: nasal secretion, bronchial mucus production, pruritic, bronchoconstriction

H2: increase gastric secretion

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26
Q

Vasopressin receptor function

A

V1: vascular sm.m. contraction
V2: increase reabsorption in collecting tubules of kidney

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27
Q

Gq activation cascade

A

Phosphorylase C –> PIP2

  1. IP3 increases Ca2+
  2. DAG activates PKC

“Cutesies HAVe 1 M and M”
Q-C
H1, a1, V1, M1, M3

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28
Q

Gs activation cascade

A

stimulate adenylyl cyclase –> increased cAMP - activates PKA

“everything else” - B1, B2, D1, H2, V2 - need other mnemonics

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29
Q

Gi cascade

A

inhibits adenylyl cyclase –> decreased cAMP and less activated PKA

MAD 2s
M2, a2, D2

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30
Q

Draw Michaelis-Menton and Lineweaver Burk plots for competitive, noncompetitive and no inhibition

A

Page 136-137

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31
Q

How does a competitive inhibitor impact Vmax and Km?

A

no change to Vmax, shifts right as increases Km

it’s competitive, takes longer to hit Vmax because it has to compete with the inhibitor

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32
Q

How does noncompetitive inhibitors impact Vmax and Km?

A

decreases Vmax, does not change Km

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33
Q

Write out the 4 pharmacokinetic equations

A

Vd = D/C

Cl= 0.7xVd/t1/2

LD: Css x Vd

MD: Css x Cl

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34
Q

how does potency and efficacy change with competitive and noncompetitive antagonists compared to full agonists?

A

Competitive: takes longer to reach same efficacy. Same efficacy, decreased potency

Noncompetitive: lower max effect, efficacy decreases

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35
Q

How do partial agonists change potency and efficacy compared to full agonist?

A

partial agonists have lower efficacy than a full agonist

Potency is independent of efficacy. Can be increased or decreased.

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36
Q

How do you calculate therapeutic index and what is the significance?

A

LD50: lethal dose to 50%
ED50: efficacy dose to 50%

TI = LD50/ED50

You want a high index or wide therapeutic window. need higher dose to kill someone OR the effective dose is small enough there is less chance of toxicity.

Wide window or high index = safer drug

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37
Q

Some Drugs With Low Therapeutic Index

A 
Seizure drugs
Digoxin
Warfarin
Lithium
Theophylline
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38
Q

Tetralogy of Fallot

A
  1. RV outflow obstruction - pulmonic stenosis
  2. RV hypertrophy
  3. VSD
  4. Overriding aorta
    “IHOP”

R to L may be intermittent and have mostly L to R = cyanotic

Crying, feeding, increased activity = R to Left = cyanotic

Squatting relieves cyanotic sx, increase systemic resistance forces L to R shunt

Boot shaped heart on CXR

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39
Q

Cardiac Output: equation and what increases or decreases it

A

SV X HR

Increased:
Exercise, increased HR (to a point)
Increased contractility - Catecholamines

Decreased:
B1 blockers
HF, acidosis, hypoxia, hypercapnia
Non-dihydropyridines - verapamil

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40
Q

Fick principle

A

CO = rate of O2 consumption/(arterial O2 - venous O2 content)

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41
Q

Mean arterial pressure (MAP)

A

P=QR MAP=(CO) x (peripheral resistance)

MAP = 2/3 diastolic + 1/3 systolic at resting HR

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42
Q

Pulse pressure

A

Systolic pressure - diastolic pressure

Increase SV increases pulse pressure

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43
Q

Ejection fraction

A

SV/EDV

Decrease in systolic HF
Increased in increased contractility

Normal 55-70%

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44
Q

Illustrate the Starling Forces affecting capillaries

A

page 177

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45
Q

Conditions causing increased hydrostatic pressure in capillaries

A

increased central venous pressure - CHF
venous thrombosis
compression of vein
sodium/water retention

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46
Q

Conditions decreasing oncotic pressure in capillaries

A

liver dz
protein malnutrition
nephrotic sn
protein losing enteropathy

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47
Q

Conditions increasing capillary permeability (Kf)

A

septic shock
toxins
burns

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48
Q

conditions increasing oncotic pressure of interstitium

A

lymphatic obstruction

-tumor, inflammation, surgery, radiation

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49
Q

Draw out the changes seen in pressure-volume loops with increasing after load, preload, and contractility.

A

page 181

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50
Q

S1 sound

A

M and T close

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51
Q

S2 sound

A

A and P close

Splitting on expiration never normal - pulmonic stenosis, RBBB

Fixed splitting - ASD

Paradoxical splitting - AS, LBBB

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52
Q

Bedside maneuvers changing mumurs

A

Inhale - increases tricuspid M
Exhale - increases mitral M

Hand grip - louder mitral regurgitation

Valsalva - most get softer, makes hypertrophic cardiomyopathy M louder

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53
Q

Aortic regurgitation

A

Early Diastolic M, decrescendo

Wide pulse pressure
Water hammer pulse - strong bounding peripheral pulses
Head bobbing

Causes:
Dilation aortic root - tert syphilis, marfans
Bicuspid aortic valve
Rheumatic fever

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54
Q

Mitral Stenosis

A

Diastolic M - opening snap

enhanced by expiration

Cause:
Rheumatic HD

–> L atrial dilation

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55
Q

Mitral regurgitation

A

Holosystolic M

Radiates to left axilla

Increased in hand grip, squatting

Causes:
Rheumatic heart dz
endocarditis
ischemic heart dz
LV dilation - separate valve leaflets
Mitral valve prolapse
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56
Q

Tricuspid regurgitation

A

Holosystolic M
Louder w/ inspiration - distinguishes from MR

Cause:
Rheumatic heart dz
endocarditis - IV drug users

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57
Q

Ventricular septal defect murmur

A

holosystolic M - left sternal border by T

NEWBORNS!

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58
Q

Aortic Stenosis

A

Systolic M w/ ejection click, crescendo, decrescendo

Radiates to carotids
Weak, delayed peripheral pulses –> syncope

angina, dyspnea

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59
Q

What causes the dicrotic notch in the pressure tracing of the cardiac cycle?

A

elasticity of the aorta causes increase in pressure as the valve closes - dips is the back flow as the valve closes and the coronary artery fills

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60
Q

What accounts for the a, c, and v waves in the atrial pressure (aka venous pulse)?

A

a: Atrial contraction against an increasing ventricle pressure
c: Ventrical contraction causes valves to bulge into atria
v: filling against closed M/T valves

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61
Q

When does the isometric contraction fall in the cardiac cycle?

A

between the AV valves (M/T) closes - S1 heart sound

and the aortic valve opens

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62
Q

When does isometric relaxation fall in the cardiac cycle?

A

between Aortic valve closing - S2 heart sound

and AV valves (M/T) opening

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63
Q

What is happening in the heart during diastole? What are the phases called

A
  1. Isometric relaxation
  2. rapid flow
  3. diastasis
  4. atrial systole
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64
Q

S3 heart sound

A

early-mid diastole during rapid ventricular filling

Common in dilated ventricles - dilated cardiomyopathy, CHF
Mitral regurg
L to R shunt - VSD, ASD, PDA

Normal in kids and pregnant women (increased preload)

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65
Q

S4 heart sound

A

right before S1

atrial kick

high atrial pressure in ventricle hypertrophy

  • hypertrophic cardiomyopathy
  • aortic stenosis
  • chronic HTN w/ LVH
  • post MI
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66
Q

What causes a normal splitting of S2?

A

Inhalation - decreases intrathoracic pressure which sucks blood into the RA, increases preload to RV

More to push out causes slight delay in pulmonic valve closure

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67
Q

What causes wide splitting S2?

A

expiration splitting of S2 is never normal

caused by pulmonic stenosis, RBBB

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68
Q

What causes paradoxical splitting of S2?

A

aortic stenosis, LBBB

P2 delay - improved in inspiration

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69
Q

What causes fixed splitting of S2?

A

atrial septal defects - more blood into R heart through L to R shunt

slower expel of blood from RV and closure of pulmonic valve

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70
Q

What heart sounds/murmurs are heard better in the left lateral decubitus position?

A

MS, MR, left-sided S3, S4

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71
Q

Draw out the diastolic heart murmurs

A

page 185

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72
Q

Draw out the systolic heart murmurs

A

page 188

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73
Q

Osteoporosis

A

Increased resorption of bone, decreased osteoblast activity
Prone to fx, spinal compressive fx –> increased kyphosis
Dx w/ DEXA scan

Tx:
stop smoking, stop steroids if able, increase exercise
Ca/vit D supplementation
Bisphosphonates (inhibit osteoclastic resorption, risk erosive esophagitis, osteonecrosis of jaw)
Conjugated estrogen
SERM (raloxifen)
Teriparatide (pulsatile injections not to exceed 2 yrs)
Denosumab (RANK-L inhibitor)

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74
Q

Serum Ca2+, Serum phosphate, alk phos and PTH levels in osteoporosis

A

all normal

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75
Q

Serum Ca2+, Serum phosphate, alk phos and PTH levels in osteopetrosis

A

generally normal, can have slight increase in PTH and alk phos (osteoblast activity marker) and slight decrease in Ca2+

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76
Q

Serum Ca2+, Serum phosphate, alk phos and PTH levels in paget disease

A

increased alk phos, rest normal

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77
Q

Serum Ca2+, Serum phosphate, alk phos and PTH levels in rickets/osteomalacia

A

Vit D deficiency –> decreased serum Ca2+, which increases PTH that dumps serum phos into urine (so decrease serum phos), alk phos is either normal or slightly increased

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78
Q

Serum Ca2+, Serum phosphate, alk phos and PTH levels in Renal insufficiency

A

Can’t activate VitD –> decreased serum Ca2+, increased PTH, but kidney can’t dump phosphate so increased serum phos and alk phos is either normal or increased

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79
Q

Serum Ca2+, Serum phosphate, alk phos and PTH levels in Vit D intoxication

A

Serum Ca2+ high, PTH low, Serum Phos high, alk phos normal

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80
Q

Serum Ca2+, Serum phosphate, alk phos and PTH levels in Primary hyperparathyroidism

A

High PTH, increases serum Ca2+ and alk phos, low serum phos

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81
Q

Serum Ca2+, Serum phosphate, alk phos and PTH levels in osteitis fibrosa cystica

A

Caused by high PTH:

high PTH, high serum Ca2+, low serum Phos, high alk phos

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82
Q

Hand manifestations of RA

A

Swan neck deformity - PIP hyperextension w/ compensatory flexion of the DIP

Boutonniere deformity - flexion contracture of the PIP and extension of the DIP

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83
Q

Wrist manifestations of RA

A

radial deviation at the wrist with ulnar deviation of the digits

Deformity resulting in median n. entrapment - carpal tunnel syndrome

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84
Q

Elbow manifestations of RA

A

flexion contractures

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85
Q

Knee manifestations of RA

A

synovial hypertrophy w/ chronic effusion and ligamentous laxity

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86
Q

Posterior knee manifestations of RA

A

Popliteal (Baker’s) cyst- extension of the inflamed synovium into the popliteal space

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87
Q

Ankle, forefoot, subtalar manifestations of RA

A

deformities, pain w/ ambulation

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88
Q

Upper cervical spine manifestations of RA

A

Atlantoaxial subluxation

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89
Q

Location of rheumatoid nodules

A

olecranon bursa
proximal ulna
achilles tendon
occiput

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90
Q

Gout crystals

A

monosodium urate

needle shade crystals, negatively (yellow) birefringent

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91
Q

Causes of gout

A

decreased excretion of uric acid - thiazide or loop diuretics

increased production of uric acid: purine-rich foods, Lesch-Nyhan syndrome, tx for leukemia or lymphoma (increased cell turnover)

Dietary excess
Alcohol consumption - competes w/ uric acid excretion sites in kidney

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92
Q

Presentation of gout

A

asymmetric joint inflammation, inflammation in first MTP (podagra)

Top - ear, tendons, bursa - not tender

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93
Q

Most common forms of skin cancer

A
  1. basal cell
  2. squamous cell
  3. melanoma
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94
Q

Order of metastatic risk of most common forms of skin cancer

A
  1. melanoma
  2. squamous cell
  3. basal cell
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95
Q

Squamous cell carcinoma

A

sun exposed areas
locally invasive
ulcerative red lesion

Histo: keratin pearl

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96
Q

Basal cell carcinoma

A

sun exposed areas
Rolled edge appearance, central ulceration, pearly papule appearance w/ telangectasias

micro: palisading nuclei

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97
Q

Melanoma

A 
S100+
sun exposed areas
Depth of tumor correlates w/ risk of mets
-excisional w/ margins
-punch bx - full thickness

Micro: nests of melanocytes fill dermis, obscure epidermal border as goes into epidermis

ABCDs:
Asymmetry
Border irregular
Color - multiple
Diameter >pencil head
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98
Q

Homolog of glans penis

A

glans clitoris

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99
Q

Homolog of corpus spongiosum and corpora cavernosa

A

vestibular bulbs

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100
Q

Homolog of bulbourethral (Cowper) glands

A

greater vestibular (Bartholin) glands

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101
Q

Homolog of prostate gland

A

urethral and paraurethral (Skene) glands

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102
Q

Homolog of ventral shaft of penis

A

labia minor

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103
Q

Homolog of scrotum

A

labia majora

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104
Q

Female genitalia development pathway

A

No mullerian inhibitor factor = paramesonephritic ducts become fallopian tubes, uterus, upper vagina

No testosterone = mesonephric duct degenerates

No DHT= urogenital sinus becomes lower vagina

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105
Q

Male genitalia development pathway

A

SRY gene on Y Chr - testis determining factor:

  1. Sertoli cell development and secretion of mullerian inhibitory factor
    - paramesonephric (mullerian) duct degenerates
  2. Leydig cells secrete testosterone –> mesonephric duct becoming internal genital structures (except prostate)

5-alpha-reductase converts T into DHT
–> urogenital sinus becomes external genital structures and prostate

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106
Q

PCOS diagnostic criteria

A

2 of 3:
-oligo/an ovulation - menstrual irregularity, infertility
Hyperandrogenism - acne, hirsutism
Polycystic ovaries on US - string of pearls sign

Assoc sx: obesity, insulin resistance, infertility

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107
Q

Cancer risk associated with PCOS

A

increases risk of endometrial hyperplasia and cancer

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108
Q

Hormonal abnormalities in PCOS

A

Increased LH:FSH >2:1
Increased insulin
Increased estrone
Decreased sex hormone binding globulin (SHBG)

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109
Q

Cause of increased androgens in PCOS

A

LH:FSH >2:1
-LH stimulates theca cells to produce androstenedione, FSH does not stimulate granulosa cells to the same extent, not all can be converted to estradiol –> increased androgens

Increased insulin d/t insulin resistance - insulin stimulates theca cells to produce androstenedione –> androgens

Androgens and insulin suppress liver production of sex hormone binding globulin (SHBG) –> increased circulating free hormones (estrogen and androgens)

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110
Q

Cause of increased estrone in PCOS

A

Peripheral conversion of androgens to estrone in adipose tissue

prevents normal ovulatory cycle, stimulates endometrium

SHBG decreased –> increased free hormone circulating

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111
Q

Tx of PCOS

A

Diet/exercise - wt loss to reduce estrone production

OCPs
Cyclic prostestins

hirsutism:
Spironolactone -inhibits steroid binding
Ketoconazole - inhibits steroid synthesis by blocking desmolase

Metformin - insulin resistance

Clomiphene - SERM for anovulation

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112
Q

Klinefelter Syndrome

A

47, XXY - have barr body

Testicular atrophy = decrease in T, less muscle mass, less facial/body hair, broader hips

Tall, longer extremities, gynecomastia, female hair distribution

Reduced fertility - dysgenesis of seminiferous tubules - decreased inhibin, increased FSH

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113
Q

Turner Syndrome

A

MC cause of primary amenorrhea

45, XO - no barr body

Short stature, shield chest, low hairline, low set ears, webbing of neck (cystic hygroma)

gonadal dysfunction - streak ovaries = amenorrhea, infertility

Bicuspid aortic valve, coarctation of aorta

horseshoe kidney

decreased estrogen –> Increased LH and FSH

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114
Q

Label brachial plexus

A

page 91

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115
Q

Long thoracic N.

A

innervates serrates anterior m. - holds scapula on thorax

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116
Q

Supra scapular n.

A

innervates:
infraspinatus - externally rotates humerus, stabilizes joint

supraspinatus m. - abducts arm

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117
Q

Lateral pectoral N.

A

innervates pectoralis m. - flexion, adduction, medial rotation of humerus

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118
Q

Upper scapular N.

A

subscapularis m. - internally rotate arm

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119
Q

Thoracodorsal N.

A

Latissimus dorsi m. - extension, adduction, transverse extension, flexion from extended position and internal rotation

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120
Q

Lower sub scapular N.

A

teres major - medially rotates and adducts arm

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121
Q

Musculocutaneous N

A

biceps, coracobrachialis, branchialis m. - main flexors of arm

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122
Q

Axillary N.

A

deltoid - abduct in frontal plane

teres minor - laterally rotate humerus

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123
Q

Radial N.

A

extensors and triceps - extend forearm

injury –> wrist drop

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124
Q

Median N.

A

pronators and thenar m. of hand - pronate forearm

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125
Q

Ulnar N.

A

interosseous, hypothenar m of hand, flexor carpi ulnas m.

flex and adduct hand

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126
Q

Erb duchenne palsy

A

Waiter’s tip
Lesion of the superior trunk (C5-C6) - bruising, stretching, or tearing (permanent) of N.
Trauma - shoulder/neck d/t shoulder dystocia or clavicle fracture in birth

damage to supra scapular N., musculocutaneous n., axillary n.

complete or partial paralysis of UE

Adducted, medially rotated, pronated forearm

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127
Q

Klumpke’s palsy

A

Lesion of inferior trunk (C8-T1)
traction of abducted arm

paralysis/atrophy of intrinsic m. of hand - hypothenar/thenar, interosseous m.
+/- wrist/finger flexors

Sensory defects - medial arm, forearm, hand

Severe: supination of forearm w/ wrist and fingers flexed

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128
Q

Lymphatic draining of arm, lateral breast

A

axillary nodes

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129
Q

Lymphatic draining of posterior calf, dorsolateral foot

A

popliteal nodes

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130
Q

Lymphatic draining of thigh

A

superficial inguinal nodes

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131
Q

Lymphatic draining of stomach, upper duodenum

A

celiac nodes

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132
Q

Lymphatic draining of lower duodenum, jejunum, ileum, proximal 2/3 of colon

A

superior mesenteric nodes

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133
Q

Lymphatic draining of distal 1/3 of colon, upper rectum

A

inferior mesenteric nodes

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134
Q

Lymphatic draining of lower rectum (bladder, cervix, prostate too) (above pectinate line)

A

internal iliac nodes

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135
Q

Lymphatic draining of anal canal (below pectinate line)

A

superficial inguinal nodes

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136
Q

Lymphatic draining of testes, ovaries, uterus, kidneys

A

para-aortic nodes

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137
Q

Lymphatic draining of scrotum, vulva

A

superficial inguinal nodes

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138
Q

Lymphatic draining of right arm and right half of head? Rest of body?

A

right lymphatic duct

Thoracic duct to junction of left subclavian v/l internal jugular vain

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139
Q

Antibody structure

A

Fab - antigen binding region
-idiotype
2 light chains, 2 heavy chains

Fc - constant region, heavy chains only

  • carboxy terminal
  • compliment binding
  • recognized by CD16 on NK cells
  • determines isotypes
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140
Q

Ab heavy chains

A 
mu - IgM
delta - IgD
gamma - IgG - (gamma 2 lambda 2 or gamma 2 kappa 2)
alpha - IgA
epsilon - IgE
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141
Q

Ab light chains

A 
lambda and kappa
2 kappa:1 lambda normally
-ratio important in dx multiple myeloma
-proliferation of 1 malignant plasma cell produces all same Ab
-ratio will skew
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142
Q

Circulating IgG

A 
Most abundant in blood
delayed secondary immune response
fixes complement
crosses placenta
opsonizes bacteria
binds/neutralizes viruses and bacteria toxins
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143
Q

Circulating IgA

A

mucous membranes and Gi tract - MALT
monomer in circulation
secretory IgA is a dimer (end to end) - GI tract, tears, mucus, saliva, breast milk

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144
Q

IgA to lumen

A

transcytosis

-as it passes through cells, picks up secretory component that protects the dimer from gastric acid

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145
Q

Circulating IgE

A

parasite immunity by activating eosinophils
bind receptors on mast cells and basophils
–> cross linking –> degranulate

Type I hypersensitivity reaction - allergies

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146
Q

IgM

A

surface of B cells - monomer
circulation - pentamer

primary immune response - early
-used as a marker for acute illness

does not cross placenta

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147
Q

IgD

A

surface of B cells

low level in serum

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148
Q

V(D)J recombination

A

Rearrangement of DNA segments:

  • variable (V)
  • diversity (D)
  • joining (J)

rearrangement begins w/ dsDNA breaks at recomination signal sequences (RSSs) that flank V, D, J coding regions

V(D)J recombination initated by recombination activating gene complex (RAG-1 and RAG-2)
-RAG-1 and RAG-2 recognize RSSs

Mutations in RAG genes –> inability to initiate VDJ rearrangements
–> arrest B and T cell development

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149
Q

Anti-IgG Antibodies

A

aka rheumatoid factor

RA - nonspecific

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150
Q

Anti-citrullinated protein Ab (ACPA)

A

RA - specific

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151
Q

Antinuclear antibodies (ANA)

A

SLE - nonspecific

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152
Q

Anti-Smith

A

SLE - specific

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153
Q

Anti-dsDNA

A

SLE renal disease

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154
Q

Anti histone

A

Drug induced lupus “SHIPP”

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155
Q

Anti centromere

A

CREST scleroderma (limited)

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156
Q

Anti-Scl-70

A

aka anti-DNAtopoisomerase

Diffuse scleroderma

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157
Q

Anti-Jo-1

A

Polymyositis/dermatomyositis

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158
Q

Anti SSA (anti Ro)

A

Sjogrens

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159
Q

Anti SSB (anti La)

A

Sjogrens

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160
Q

Anti-U1-RNP (Ribonucleoprotein)

A

mixed connective tissue disease

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161
Q

Anti-desmoglein

A

pemphigus vulgaris

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162
Q

Anti-acetylcholine receptor

A

myasthenia gravis

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163
Q

Anti-endomysial (anti tissue transglutaminase)

A

celiac disease

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164
Q

Anti-gliadin

A

celiac disease

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165
Q

Anti-mitochondrial

A

primary biliary cholangitis

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166
Q

Anti-smooth muscle

A

autoimmune hepatitis

167
Q

Anti-glutamate decarboxylase

A

T1DM

168
Q

Anti-thyrotropin reeptor

A

graves dz

169
Q

antithyroid peroxidase (anti TPO)

A

hashimoto thyroiditis

170
Q

Antithyroglobulin

A

hashimoto thyroiditis/graves dz

171
Q

anti-basement membrane

A

good pasture syndrome

172
Q

c-ANCA (PR3-ANCA)

A

granulomatosis w/ polyangitis “wegners”

173
Q

p-ANCA (MPO-ANCA)

A

pauci-immune crescentric glomerulonephritis
churg-strauss syndrome
microscopic polyangiitis

174
Q

Type I Hypersensitivity Reaction

A

IgE, mast cells, basophil mediated

Free Ag binds IgE on presensitized mast cells and basophils

Release of preformed granules of histamine and bradykinin

  • -> vasodilation
  • -> increased vascular permeability

wheal and flare reaction - utricaria “hives”

Rapid

Anaphylaxis

Atopic disorders - asthma, eczema, allergic rhinitis

175
Q

Type II hypersensitivity Reaction

A

Ab against cellular Ag

Complement mediated damage
M0 phagocytosis
NK cell destruction

Autoimmune hemolytic anemai
acute hemolytic transfusion reaction
Erythroblastosis fetalis - IgG of mom attacks fetal RBCs
Immune thrombocytopenia (ITP) - attack platelets
Pernicious anemia - Ab against IF
Myasthenia gravis
Guillian Barre syndrome - Ab against schwann cells
Graves dz
Pemphigus vulgaris
Bullous pemphigoid
Good pastures Sn
Acute Rheumatic fever
176
Q

Type III hypersensitivity reaction

A

Ab-Ag complexes

Ab against soluble Ag –> complex deposition in tissues
activation of complement
recruit of N0

SLE, RA
polyarteritis nodosa
post strep GN
serum sickness - Ab mediated drug reaction
Arthus reaction - 4-12 hours after injection - locally deposited complexes

177
Q

Type IV hypersensitivity reaction

A

delayed, cell mediated

T cells bind Ag –> cytokines
–> M0 activation, tissue damage

PPD
Poison ivy --> contact dermatitis
hashimoto thyroiditis
MS
graft vs host disease
178
Q

Thymic aplasia

A

DiGeorge

3rd and 4th pharyngeal pouches fail to develop

  • no thymus –> no mature T cells
  • no parathyroids –> low PTH –> hypocalcemia and tetany (positive Chvostek and Trousseau signs)

Recurrent viral, fungal, protozoal infections

congenital defects in heart, great vessels

90% have 22q11 deletion - detect with FISH

179
Q

Chronic mucocutaneous candidasis

A

t cell dysfunction vs C. albicans

tx: ketoconazole

180
Q

IL12 receptor deficiency

A

produced by M0 to Th0-Th1

mycobacterial and fungal infections

181
Q

Bruton agammaglobulinemia

A

X linked (boys)

B cell deficiency –> defective tyrosine kinase gene –> low levels of all Igs

recurrent bacterial infections after 3-6 mo old - protected by mom’s IgG

182
Q

Selective immunoglobulin deficiencies

A

IgA deficiency MC

  • most appear healthy
  • sinus and lung infections
  • 1/600 European descent
  • Assoc w/ atopy and asthma
  • possible anaphylaxis to blood transfusions and blood products
183
Q

Severe combined immunodeficiency (SCID)

A

X linked

defect in early stem cell differentiation

Adenosine deaminase deficiency

Last defense is NK cells

Presentation triad:

  1. Severe recurrent infections
    - chronic mucocutaneous candidiasis
    - Fatal or recurrent RSV, VZV, HSV, measles, flu, parainfluenza
    - P. jirovecii pneumonia (PCP)
  2. chronic diarrhea
  3. failure to thrive

no thymic shadow on newborn CXR

184
Q

Ataxia-telangectasia

A

IgA deficiency and T cell deficiency –> sinus and lung infections

Cerebellar ataxia and poor smooth pursuit of moving target with eyes

Telangectasias of face after 5 yo

Radiation sensitivity - avoid Xrays

Increased risk: lymphoma and acute leukemias

Elevated AFP - after 8 mo of age

Average age of death - 25 yrs

185
Q

Wiskott-Aldrich syndrome

A

WAITER

  • Wiskott
  • Aldritch
  • Immunodeficiency
  • Thrombocytopenia and purpura
  • Eczema
  • Recurrent pyogenic infections

X linked
No IgM vs bacterial capsular polysaccharides

Low IgM, high IgA

186
Q

Hyper-IgM syndrome

A

B and T cell issue

Increased IgM - other Ab isotypes decreased

AR –> no CD40 on B cells
X linked –> no CD40 ligand on helper T cells (MC)

187
Q

Chronic granulomatous disease (CGD)

A

X linked 65-70%

Lack NADPH oxidase –> phagocytes cannot destroy catalase + microbes

Susceptible to S. aureas, aspergillus infections

Tx: prophylactic TMP-SMX and itraconazole

IFN-gamma helpful

188
Q

Chediak - Higashi syndrome

A

Defective LYST gene - lysosomal transport

Defective phagocyte lysosomes –> giant cytoplasmic granules in PMNs diagnostic

Triad:

  • partial albinism
  • recurrent respiratory tract and skin infections
  • neurologic disorders
189
Q

Hyper-IgE syndrome (Job syndrome)

A

Mutation in STAT3 gene

  • -> impaired differentiation of Th17 cells - recruit N0 to fight opportunistic infections
  • -> impaired recruitment of neutrophils

High levels of IgE and eosinophils

triad:
-eczema
recurrent COLD S. aureas abscesses
Coarse facial features: broad nose, prominent forehead (bossing), deep-set eyes, “doughy” skin

Most common: retained primary teeth –> 2 rows of teeth

190
Q

Leukocyte adhesion deficiency syndrome

A

Abnormal integrins –> inability of phagocytes to exit circuation

delated separation of umbilical cord - couple months

191
Q

Aorta branches - anterior trunks

A

Celiac - foregut
Superior mesenteric artery - mid gut
Inferior mesenteric artery - hind gut

192
Q

Splenic flexure watershed

A

affected first w/ systemic hypotension

shock –> ischemia

193
Q

Abdominal CT

A

Tail of pancreas “tickles” hilum of spleen

IVC to right of aorta

review abdominal CT links on GI5

194
Q

Celiac disease

A

autoimmune

intolerance of gliadin (gluten and wheat)
Ab to gliadin and tissue transglutaminase

Blunting of villi and microvilli

Impaired absorption

  • foul smelling, pale stool
  • stunted growth
  • failure to thrive

HLA-DQ2, HLA-DQ8

Increased risk of T cel lymphoma, GI cancer, breast CA

195
Q

Crohn’s disease (except pharma tx)

A

Inflammation of “Everything”

  • transmural
  • mouth to anus
  • MC: terminal ileum

Skip lesions
Spares rectum

Assoc: intestinal flora - tx probiotics

Barium swallow : string sign - narrowed lumen d/t inflammation

Stricturing
Diarrhea
malabsorption
wt loss
increased risk of colon CA (not as high as UC)

Fistulas - enterocolic, enterovasicular, enterovaginal, enterocutaneous

HLA-B27 disorder: arthritis, joint problems

Immunologic problems

Erythema nodosum -painful red SQ nodules on shins

Bx: noncaseating granulomas

196
Q

Treatment of crohn’s disease

A

5-ASA agents: decreased production of PG in lumen; usual initial tx for mild disease

  • mesalamine
  • Sulfasalazine - SE: malaise, decreased sperm count

Azathioprine or mercaptopurine > methotrexate

Anti-TNF agents - esp if arthritic component

  • infliximab
  • adalimumab

Steroids +/- abx for acute exacerabations

197
Q

Ulcerative colitis

A 
limited to colon
distal --> proximal
continuous (no skip lesions)
ALWAYS affects rectum
Limited to mucosa and submucosa

Autoimmune

barium enema: haustra obliterated –> lead pipe appearance

Bx: crypt abscesses, ulcerations and bleeding

Bloody diarrhea (rectum)
Malnutrition
increased risk of colon CA

Assoc w/ primary sclerosing cholangictasia
pyroderma gangrenosum
sacroiliitis, uveitis - HLA B27

Tx: salicylates - sulfasalazine
6-Mercaptopurine
Infliximab
TNF-a inhibitors
Colectomy curative
198
Q

V/Q mismatch - apex vs base

A

ventilation/perfusion

Apex of lung: V/Q >1
high ventilation, low perfusion (gravity pulls more blood to base of lung)
-physiologic dead space

Base of lung V/Q less than 1

  • perfusion and ventilation both greater at base of lung
  • perfusion higher than ventilation
  • -> shunting - deoxygenated blood, not enough O2 for all the blood

W/ exercise, pulmonary capillaries dilate –> increased perfusion, V/Q closer to 1 in apex, more uniform between apex and base

199
Q

Conditions when V/Q approaches zero

A

low ventilation, high perfusion

airway obstruction - pneumonia, pulmonary edema, lung cancer

shunt - blood leaving deoxygenated

Supplemental O2 ineffective - can’t get to the alveolia

200
Q

Conditions when V/Q move toward infinity

A

high ventilation, low perfusion

blood flow obstruction or physiologic deadspace

Supplemental O2 effective

201
Q

Takayasu arteritis

A

Granulomatous inflammation of arteries off of aortic arch
–> decreased blood flow to head and arms

“pulseless dz”

Poor pulses in extremities

Young Asian females - teens - 20s

elevated ESR

202
Q

Giant cell arteritis (Temporal arteritis)

A

MC form of vasculitis

Inflammation of branches of external carotid artery - temporal a.

elderly females

SX:
u/l HA
jaw claudication
vision loss d/t occlusion of ophthalmic a. - irreversible

Elevated ESR (can r/o if normal)

palpable tender temporal a. w/ temple wasting

assoc w/ polymyalgia rheumatica (pain and joint stiffness of neck, shoulders, hips, proximal joints)

Dx: temporal a. bx

  • multinuclear giant cells
  • grnaulomas in adventitia and media of artery

Tx: high dose steroids for several months - taper off
-prevents vision loss

203
Q

Kawasaki disease

A

“mucocutaneous LN Sn”

Infants, young kids
East Asian

Fever for 5 days “CRASH and Burn”

4 of 5: “CRASH”
Conjunctivitis - b/l non exudative, painless
Rash - trunk
Adenopathy of cervical LN
Strawberry tongue w/ diffuse erythema of mucus membranes, lips
Hands and Feet - erythema or desquamation

Potential of coronary aneurysms –> rupture –> death
thrombus –> MI

Tx:
IVIG
High dose aspirin to prevent thrombosis (exception to no aspirin to kids)

204
Q

Thromboangiitis obliterans (Buerger dz)

A

small/medium arteries and veins

smokers, male, 40s

intermittent claudication

superificial nodular phlebitis

cold sensitivity
–> pain, gangrene, autoamputation of digits

Tx: stop smoking

205
Q

Polyarteritis nodosa (PAN)

A

involves kidneys
involves visceral vessels - skin, GI tract, heart
*spares lungs

Abd pain, melena, neuralgias

Assoc w/ Hep B and Hep C

  • ANCA (+ANCA rules out)

Tx: corticosteroids +/- cyclophosphamide (lets you use lower dose of steroids)

206
Q

Henoch-Schonlein purpura (IgA vasculitis)

A

MC systemic vasculitis in childhood

50% recent URI

Rash of palpable purpura of butt and legs
Arthralgias - knees
Abd pain d/t intestinal hemorrhage
Renal dz - IgA nephropathy - nephritis, hematuria (Berger’s dz)

Temporary, self limiting

207
Q

Eosinophilic granulomatosis w/ polyangiitis (Churg-Strauss Sn)

A

Giant cells and eosinophils

Assoc w/:
asthma
sinusitis
skin lesions
peripheral neuropathy

+p-ANCA (MPO-ANCA)

208
Q

Granulomatosis w/ polyangiitis (GPA) aka Wegner’s

A

Triad:
Focal necrotizing vasculitis
Granulomas in lungs (dyspnea, hemoptysis) and upper airway - soft palate, nasal, sinuses, oropharynx
Glomerulonephritis - hematuria

Collapse bridge of nose - saddle nose

+c-ANCA

Tx: cyclophosphamide, corticosteroids

209
Q

Microscopic polyangiitis

A

Affects lungs
Affects kidneys - Pauci-immune cresentric GN

+p-ANCA

210
Q

Staphylococcus aureus toxins and actions

A

a-hemolysin/a-toxin –> hemolysis

b-hemolysin/sphingomyelinase –> hemolysis

gamma-hemolysin (leukocidin) –> toxic to leukocytes, hemolysin –> hemolysis

Delta-hemolysin/delta toxin –> toxic to erythrocytes and other cells

Panton-Valentine leukocidin –> tissue destruction w/ MRSA, affects both N0 and M0

Exfoliative toxin –> scalded skin syndrome in newborns w/in 1 wk
-act at zona granulosa of epidermis –> flaccid bullae

SUPER ANTIGENS:

  • Enterotoxins –> food poisoning (V/D)
  • TSST-1 –> release of cytokines –> TSS (high fever, hypotension, diffuse rash (looks like sunburn))
211
Q

Streptococcus pyogenes toxins and actions

A

Streptolysin O –> hemolysis (Oxygen labile) - blood agar plates, ASO titer

Streptolysin S –> hemolysis (oxygen Stable)

SUPER ANTIGEN
-Streptococcal pyogenic exotoxins type A, B, C/erythrogenic toxins –> red rash (erythro-) and fever (pyro-) of scarlet fever

Toxic shock like syndrome

(RF is Ab mediated)

212
Q

Yersinia enterocolitica toxins

A

heat stabile toxin –> increased guanylyl cyclase activity –> increased cGMP

“Pseudoappendicitis” - abd pain

213
Q

Bacillus anthracis toxins

A

Anthrax toxin:

  • Edema factor - increases adenylyl cyclase
  • Lethal factor
  • Protective antigen
214
Q

Vibrio cholerae toxins

A

Choleragen - cholera toxin –> increased adenylyl cyclase –> increased cAMP

Cl- and H20 cross into lumen of intestine –> Rice water stools

12-20 L loss of fluid/day –> circulatory collapse

HYDRATE!!!

215
Q

Bordetella pertussis toxin

A

pertussis toxin - binds and inactivates Gi proteins –> increased cAMP

216
Q

Corynebacterium diphtheriae toxin

A

Diphtheria toxin inactivates EF2 (elongation factor) –> pharyngitis w/ gray pseudomembranes

Toxin lethal in small quantity - cardiac/neuro

217
Q

Pseudomonas aeruginosa toxin

A

Exotoxin A inactivates EF2

218
Q

Shigella toxin

A

Shiga toxin - similar to Ecoli O157:H7

cleave host rRNA at adenine base in 60S ribosomal subunit –> inhibited protein synthesis –> cell death

219
Q

Enterohemorrhagic E. coli (EHEC) toxin

A

(includes O157:H7)

Verocytotoxin (Shiga toxin)

  • -> bloody diarrhea
  • -> Hemolytic Uremic Syndrome (HUS): damages renal endothelial cells causing: hemolytic anemia, thrombocytopenia, acute renal failure
220
Q

Enterotoxigenic E. coli (ETEC) toxin

A

heat labile toxin –> increased adenylyl cyclase –> increased cAMP

heat stable toxin –> increased guanylyl cyclase activity –> increased cGMP

–> watery diarrhea, leading cause of travelers diarrhea

221
Q

Mycoplasma pneumoniae

A

no cell wall
perosn to person via respiratory droplets

common cause of pneumonia in school aged kids, college students**, military recruits

presentation:
1st: malaise, HA, low grade fever
–> nonproductive cough, diffuse interstitial infiltrates
“walking pneumonia”

CXR: patchy, reticulonodular infiltrates

Dx:
cold agglutinins - IgM lyse RBCs in cold environment
PCR
Serology

Tx: empiric: macrolide - azithromycin, doxycline, fluoroquinolones

222
Q 
Bacterial meningitis CSF findings:
Opening pressure
WBC count
Differential
Protein
Glucose
Gram stain
A 
Opening pressure: up
WBC count: markedly increased
Differential: neutrophils
Protein: up
Glucose: down
Gram stain: + 70-80%
223
Q 
TB/fungal  meningitis CSF findings:
Opening pressure
WBC count
Differential
Protein
Glucose
Gram stain
A 
Opening pressure: up
WBC count: up
Differential: lymphocytes
Protein: up
Glucose: down
Gram stain: none
224
Q 
Viral meningitis CSF findings:
Opening pressure
WBC count
Differential
Protein
Glucose
Gram stain
A 
Opening pressure: normal or up
WBC count: up
Differential: lymphocytes
Protein: normal or up
Glucose: normal
Gram stain: none
225
Q

TORCHeS infections

A 
Toxoplasmosis
Other: parvo B 19
Rubella
CMV
HIV/HSV
Syphillis

Primary infection in pregnancy

  • growth retardation
  • intelectual disability
  • HSM
  • miscarriage/still birth
226
Q

Toxoplasmosis

A

Toxoplasma gondii
Cat feces
undercooked meat

Congenital infection
Triad:
chorioretinitis
hydrocephalus
intracranial calcification
227
Q

Parvovirus B19

A

adults - arthritis
kids: erythema infectiosum - fifth’s dz - slapped cheek rash

fetus:
infects RBC precursors –> severe fetal anemia
–> high output HF
–> hydrops fetalis: fluid accumulating in different parts of body, ascites, plural effusions

228
Q

Rubella

A

kids: german measles - mild fever, rash

congenital infection:
cataracts
PDA
sensorineural deafness
"blueberry muffin" rash: areas of extramedullary hematopoiesis
229
Q

CMV

A

MC TORCHeS

monolike sn in kids and adults

fetal: jaundice, HSM, sensorineural hearing loss

230
Q

TORCHeS - HIV

A

transmission prevention

  • HAART during pregnancy
  • intrapartum zidovudine
  • c-section

zidovudine prophylaxis to infant

avoid breast feeding - virus shed in breast milk

231
Q

TORCHeS - HSV

A

passed via direct contact in delivery

congenital:
vesicular rash
conjunctivitis
pneumonia
CNS dz - meningoencephalitis
disseminated dz - sepsis like

Transmission prevention:

  • suppress w/ acyclovir starting at 36 weeks
  • c-section if active infection at time of labor
232
Q

Congenital syphilis

A

25% –> death

Early manifestation - first 2 yrs of life:
hepatomegaly, elevated LFTs
Rash followed by desquamation of hands and feet
snuffles - blood tinged nasal secretions - copious
skeletal abnormalities

Late manifestations - after 2 yrs of life: scarring or deterioration
frontal bossing
interstitial keratitis - cornea scarring –> blindness
saddle nose deformity
hutchinson teeth - notching of upper incisors
perforation of hard palate
saber shin - anterior bowing of tibia

233
Q

Tx of syphilis in pregnant patient who is allergic to penicillins

A

PCN G even if allergic to PCN still best tx

desensitization of PCN, gradually build up to full tx dose

234
Q

Hepadnavirus

A

Hep B - dsDNA virus

partially ds circular DNA enter nucleus
Host polymerase makes RNA intermediate from dNA

viral reverse transcriptase makes DNA from RNA intermediate

235
Q

Pneumoconiosis

A

Fibrotic lung dz w/ inhalation of inorganic dust particles
Coal dust, asbestos, silica
M0 release mediator – fibrosis of lung as try to clear

236
Q

Coal worker’s pneumoconiosis (CWP)

A

Anthracosis – mild: black pigment in lung
-carbon particles trapped in M0 of connective tissue

Simple CWP – small fibrotic lung nodule
Complicated CWP – progressive massive fibrosis

Coal workers exposure risk: coal dust, silicon dioxide, radon –risk lung cancer

237
Q

Silicosis

A

Inhaling silicon dioxide
Mining, sandblasting, construction, demolition, cement/concrete production, masonry/stone cutting, foundry work, hydraulic fracturing “fracking”

M0 take up silica -> inflammation

Innumerable calcified nodules

Egg shel calcifications in hilar nodes -> progressive massive fibrosis

Increased susceptibility of TB – M0 can’t kill them
Increased risk of lung CA x2 risk

238
Q

Asbestosis

A

Shipbuilding, roofing, pipe fitting, plumbing
Spouse doing laundry

Fibers in peripheral lung – lung bases

Directly toxic to lung parenchyma

M0 release inflammatory mediators -> damage

Fibers covered w/ iron containing protein – ferruginous bodies

  • “dumbbell” shape
  • golden brown w/ Prussian blue stain

pleural plaques
pleural effusions
interstitial fibrosis

Increased cancer risk:
Laryngeal CA, malignant mesothelioma, lung cancer: squamous cell, adenocarcinoma

Bronchogenic carcinoma much more common than mesothelioma in asbestos exposure

Smoking and asbestos exposure increases lung CA risk 60 fold

239
Q

Berylliosis

A

High tech electronics, aerospace manufacturing

Noncaseating granulomas similar to sarcoidosis

Increase risk of lung CA

240
Q

Sarcoidosis

A

AA, young females 30-40s

“A GRUELING Disease”
ACE enzyme increase
Gammaglobulinemia
Rhematoid factor
Uveitis (and other ocular manifestations) vascular layer
Erythema nodosum – tibia, sq fat inflammation
Lymphadenopathy – b/l hilar
Idiopathic
Noncaseating
Granulomas
vitD increase – activated M0 in granulomas -> hypercalcemia/-uria

Tx: glucocorticoids

241
Q

Granulomatosis w/ polyangiitis aka Wegners

A

Triad:
Necrotizing granulomas of lung and upper airway
Necrotizing granulomatous vasculitis most prominent in lungs and upper airway
Focal necrotizing granulonephritis

242
Q

Central lung cancers

A

Squamous cell carcinoma of lung

Small cell carcinoma of lung

243
Q

Peripheral lung cancers

A

Adenocarcinoma

Large cell carcinoma of lung

244
Q

Lung cancer sx

A

Cough
hemoptysis
Chest pain

Wt loss
Night sweats
Pneumonia
Pleural effusion
Airway obstruction
Paraneoplastic sn
245
Q

Adenocarcinoma of lung

A

36%- MC lung cancer
Peripheral lung – pre-existing parenchymal scars

Risk factors: smoking, gene mutations “MARKER”
MET, ALK, RET, KRAS, EGFR, ROS

MC nonsmokers and females

246
Q

Squamous cell carcinoma of lung

A

20% 2nd MC lung cancer
Central lung – hilar mass in bronchus, cavitated lesion on CXR/CT

Risk factor: smoking

Histo: Keratin pearls

Can secrete PTH-related protein –> hypercalcemia

247
Q

Large cell carcinoma of lung

A

Peripheral lung
Risk factor smoking
Histo: anaplastic and undifferentiated, giant cells with various pleomorphisms

Poor prognosis

248
Q

Small cell carcinoma of lung

A

High nucleus:cytoplasm ratio
Risk: smoking
Central lung

Hormone secretion:
ACTH -> Cushing Sn
ADH -> SIADH
Ab against presynaptic Ca2+ channels -> Lambert-Eaton Sn (muscle weakness improves w/ use)

Undifferentiated, very aggressive
Poor prognosis

TP53, Rb gene mutations
Amplicfications of MYC

249
Q

Carcinoid tumor

A

1—5% lung tumors

low-grade malignant tumor secretes serotonin

Carcinoid syndrome “BFDR”
Bronchospasm and wheezing
Flushing
Diarrhea
Right-sided heart lesions (valvular lesion, murmur)

Lung and GI tract – MC tumor of appendix

75-80% pts w/ carcinoid sn have small bowel carcinoid

Most do not met

Has to be outside of GI to have sx

250
Q

Pancoast turmor

A

Apex of lung

Most non-small cell lung cancers

Horner sn (ptosis, miosis, anhidrosis)

May compress recurrent laryngeal n. -> hoarseness

251
Q

Mesothelioma

A

In pleura

Risk factor: asbestos exposure – not MC cancer w/ exposure – bronchogenic carcinoma

Poor prognosis

No smoking associations

252
Q

Lung cancer mets to other sites

A

Brain
Bone
Liver
Adrenal glands

253
Q

Lungs receive mets from

A

Breast
Colon
Prostate
Bladder

254
Q

Paraneoplastic sn assoc w/ lung cancers

A

Squamous cell carcinoma -> hypercalcemia

Small cell carcinoma -> SIADH, Cushing Sn, Lambert-Easton

255
Q

Compression complications in lung cancers

A

Hoarseness – recurrent laryngeal n. compression

Horner’s sn – Pancoast

Dysphagia – esophageal invasion

SVC syndrome – impaired drainage of blood from head

256
Q

Draw table for sensitivity, specificity, PPV, NPV

A

Pg 482

257
Q

Sensitivity

A

Number with a positive test that have the dz

258
Q

Specificity

A

Number w/o dz that tests negative

259
Q

PPV

A

Likelihood positive test = dz

260
Q

NPV

A

Likelihood – test is dz free

261
Q

How does changes in prevalence impact PPV and NPV?

A

Increase in dz Increases A = increased PPV
Decrease in dz decreases A = decreased PPV

Increased dz increases C = decreased NPV
Decreased dz decreases C = increased NPV

262
Q

Relative risk

A

Cohort study

Probability of getting dz in exposed group vs getting dz in unexposed group

A/A+B / C/C+D
If low dz = A/B / C/D

263
Q

Odds ratio

A

Approximates relative risk if low prevalence

A/B / C/D

264
Q

Attributable Risk (AR)

A

AR = incidence of dz (exposed group) – incidence of dz (unexposed group)

AR = A/A+B – C/C+D

265
Q

Absolute risk reduction

A

No intervention – intervention

ARR = C/C+D – A/A+B

Control – experimental grp

266
Q

Number needed to harm

A

1/AR

267
Q

Number needed to treat

A

NNT = 1/ARR

Number of patients you need to treat to save/affect one life

Important number to help determine if a drug should be used or is cost effective

268
Q

Precision (reliability)

A

How reproducible result is
Consistent test
No necessarily accurate

269
Q

Accuracy (validity)

A

How closely results reflect the truth

270
Q

Beneficence

A

Ethical duty to act in pt’s best interest

271
Q

Autonomy

A

Pt right to chose what’s done to them

Physician: chose what tx will or will not provide

272
Q

Nonmaleficence

A

Avoid intentionally harming pt

273
Q

Justice

A

Treat people fairly

274
Q

Privacy breaking situations

A

Child abuse
Dz reporting
Schools
Employers – record of illness

275
Q

Informed consent

A 
Understanding of:
Procedure/tx
Risk involved
Expected benefits
Alternatives
276
Q

Decision making capacity

A 
Must be able to make and communicate a decision
Informed
Decision must be:
Consistent w/ pt values and goals
Stable over time
Not based on delusions or hallucinations
277
Q

Substituted judgement

A

Substitute someone else’s consent for pt’s consent

278
Q

Advanced directives

A

Oral AD

Written AD – living will

279
Q

Durable power of attorney for healthcare

A

Make decision

280
Q

No assignment of surrogate decision maker

A

Legally assigned order:

Spouse
Adult kids
Pt parents
Siblings

281
Q

Treating minors

A

Informed consent from parents or legal guardian

Except: own conset:
16 yo, on own – emancipated
STDs
Pregnancy
Drug addiction
Child of minor
Serving sentence of confinement
Emergencies
282
Q

Failure modes and effects analysis (FMEA)

A

Proactive, systemic analysis of how a process might fail and impact of these failures in order to identify parts of process most in need of change

  1. List steps in process
  2. Identify failure modes “what could go wrong”
  3. Identify failure causes “why would the failure happen”
    Identify failure effects “what are the consequences of each failure”
283
Q

Strategies for Ethics questions

A

Always remain professional
Maintain good physician-patient relationship
Respect pts rights to privacy and autonomy

284
Q

Pregnant teen adoption/abortion

A

Can’t be forced to abort or adopt by parents

Teen wanting abortion – state laws

Most require parent notification or consent if elective and not emergent

285
Q

Financial relationships of physician

A

Unethical to get kickbacks for referring to specific facility for healthcare

Referrals to facility w/ ownership stake is unethical

286
Q

Malpractice claim components

A

Duty to provide care
Breach of duty
Harm to patient
Damage suffered (emotional, physical, financial)

MC: lack pt/dr relationship

287
Q

Autosomal Dominance heritance pattern

A

1 allele mutation cause dz
structural genes- usually

every generation effected

288
Q

Common AD disorders

A 
ADPKD
Achondroplasia
FAP
Familial hypercholesterolemia
Osler-Weber-Rendu Sx
Hereditary spherocytosis
Huntington dz
Marfan dz
MEN
NF type 1 and 2
Tuberous sclerosis
Von Hippel-Lindau dz
289
Q

Autosomal recessive heritance pattern

A

25% receive 2 recessive alleles
only in 1 generation
-enzyme deficiency usually
-not all are recessive but often are

290
Q

Common AR disorders

A 
Albinism
ARPKD
CF
Mucopolysaccharidosis
PKU
Sickle cell dz
Sphingolipioses
Glycogen storage dz
Hemochromatosis
Thalassemias
Wilson dz
291
Q

X linked recessive heritance pattern

A

Males 50% effected

Females 50% carriers

292
Q

X linked recessive disorders

A

“Oblivious Female Will Give Her Boys X-linked Disorders”

Ocular albinism
Fabry dz
Wiskott-Aldrick
G6PD deficiency
Hunter Sn
Bruton alpha-gammaglobinemia

Hemophila A and B
Lesch-Nyhan Sn
Duchenne muscular dystrophy

293
Q

Review inheritance diagrams

A

Pages 524-525

294
Q

Mitochondrial inheritance defects

A

Mitochondrial myopathies – ragged-red muscle fibers on bx

Leber hereditary optic neuropathy
Leigh syndrome – subacute sclerosing encephalopathy

Only female offspring affected

295
Q

X linked dominant

A

Transmitted though both
All females of affected male will have it

Ex: fragile X syndrome

296
Q

Anticipation

A

Age of onset earlier and earlier in successive generations

Or severity of dz worsens w/ successive generations

297
Q

Codominance

A

2 alleles neither dominant (ABO)

298
Q

Variable expression

A

Severity of phenotype varies from 1 to another

Ex: tuberous sclerosis

299
Q

Pleiotropy

A

Single gene has more than 1 effect on phenotype (PKU)

300
Q

Locus heterogeneity

A

Mutaitons of different loci -> same phenotype

Marfan, MEN2B, homocysteinuria
-> same marfanoid body habitus

301
Q

Mosaicism

A

Cells in body w/ different genetic makeup

302
Q

Imprinting

A

Phenotype differences depend on if mutation from mom or dad genes

Prader Willi vs Angelman sn

303
Q

Prader-Willi Sn

A

“Papa”

Deletion of Proximal Portion of Chr 15q11-q13 from Paternal origin

Infant: hypotonia, poor feeding, characteristic facial features (almond-shaped eyes, downward turned mouth)

Sx: hyperphagia, obesity, short stature (partial GH deficiency), intellectual disability, behavior disorders (tantrums, skin picking, OCD), hypogonadotropic hypogonadism -> genital hypoplasia, osteoporosis in childhood, delayed menarche

Dx: confirmed w FISH

Tx: limit access to food, GH if short stature

304
Q

Angelman syndrome

A

Deletion of Chr 15
Paternal inactivated, maternal deleted
Intellectual diability, seizures, inappropriate laughter “happy puppet”
Ataxic gate

305
Q

Prader willi vs Angelman

A

POP:
Prader willi
Obesity/Overeating
Paternal gene

MAMA:
Maternal gene
Angelman (Angel MOM)
Mood- happy, laughter
Ataxia
306
Q

Hardy-weinberg population genetics

A

P+q =1

P2 + 2pq + q2 = 1

307
Q

Review gel electrophoresis and DNA sequences

A

Page 528

308
Q

Draw out phenylalanine derivative pathway

A

Page 556

309
Q

PKU

A

Deficient in phenylalanine hydroxylase OR cofactor tetrahydrobiopterin (BH4)

Tyrosine becomes essential aa

Avoid phenylalanine -> phenoketones: phenyl-acetate, -lactate, -pyruvate

Growth retardation
Intellectual disability
Seizures
Fair skin
Eczema
MUSTY body odor

Screen 2-3 days old

Tx: avoid phenylalanine: aspartame, diary products, meat, fish, chicken, eggs, beans, nuts
Add tyrosine into diet
+/- BH4
w/ in 3 wks of life

310
Q

PKU mom –non managed effects on baby

A

Microcephaly
Intellectual disability
Growth retardation
Congenital heart defects

311
Q

Vit D toxicity

A

Hypercalcemia

-assoc w/ sarcoidosis: M0 in granulomas increase conversion to active form of Vit D

312
Q

Draw vitamin D activation pathway

A

Page 561

313
Q

Vitamin K

A

Post translational modification of various clotting factors
-synthesized by intestinal floral

diSCo 1972: Protein C, S, factors 10, 9, 7, 2

decrease w/ warfarin

314
Q

Vit K deficiency

A

Warfarin
Anticonvulsants – phenytoin
Abx: wipe out gut flora

Newborns have problems with hemorrhage

  • sterile gut, can’t make vit K
  • give single vit K injection at birth
315
Q

Vit D deficiency

A

Inadequate dietary Vit D – breast milk not adequate enough Vit D – supplement

Impaired hydroxylation to make 25-OH vit D in liver
Impaired kidney hydroxylation to make 1,25-(OH)2 Vit D
End organ insensitivity to Vit D

Sx: kickets – kids; osteomalacia adults

Bone tenderness
Muscle weakness
Skeletal deformity
Bowing of legs
Growth problems
Pathologic fx
Dental problems
316
Q

Vit A

A

Retinol – eye and immune system, maintenance of epithelial cells and mucus secreting cells

Retinal
B-carotene – cleaved to 2 retinols
Retinoic acid – unusable tx

Use:
Decrease size and secretion of sebaceous glands:
mild to mod acne – tretinoin
Severe acne – oral isotretinoin

Measles
AML – M3 subtype

Pregnancy – risk teratogenicity w/ supplementation

317
Q

Vit A deficiency

A

Night blindness
Xerophthalmia -> corneal ulceration and blindness
Keratomalacia – wrinkling and clouding of cornea
Bitot spots – silver/gray plaques on conjunctiva

318
Q

Vit A toxicity

A 
HA
N/V
Stupor
Increased ICP – pseudotumor cerebri
Dry and pruritic skin
Hepatomegaly
\+/- cirrhosis
bone and joint pain
alopecia
319
Q

Vit E – alpha-tocopherol

A

Antioxidants esp RBCs

Deficient:
Hemolytic anemia
Spinocerebellar degeneration -> ataxia
Peripheral neuropathy
Proximal m. weakness
320
Q

Vit C ascorbic acid

A

Hydroxylation of prolyl and lysyl residues of collagen
Regulate dopamine -> NE by dopamine beta-hydroxylase
Antioxidant – protect RBCs
Facilitates iron absorption in gut

Deficiency – scurvy
Sore, spongy gums
Loose teeth
Fragile blood vessels
Swollen joints
Hemarthrosis
Impaired wound healing
Anemia
321
Q

Diagnostic sx of major depressive disorder

A

5/9 sx:

DIGS CAPES
At least 1:
Depressed mood
Interest diminished – anhedonia

Guilt or worthlessness
Sleep disturbances – increased or decreased
Concentration impaired
Appetite or wt changes (up or down)
Psychomotor agitation or retardation
Energy loss – fatigue
Suicidal ideation – recurrent thoughts of death – preoccupation w/ death

322
Q

Cluster A personality disorders

A

Paranoid
Schizoid
Schizotypal

“weird ones”
no psychosis

323
Q

Paranoid personality disorder

A

Long standing suspiciousness and generalized distrust of others

Use projection

324
Q

Schizoid personality disorder

A

Voluntary social withdrawal

Limited emotional expressions

325
Q

Schizotypal personality disorder

A

Eccentric appearance
Odd beliefs
Magical thinking

326
Q

Cluster B personality disorders

A

All about drama, scary

Antisocial
Borderline
Histrionic
Narcissistic

327
Q

Antisocial personality disorder

A

M>F
Disregard for and violation of others rights
-> criminality
lack empathy

328
Q

Borderline personality disorder

A

Unusual variablility and depth of mood
Unstable mood
Chaotic interpersonal relationships
Manipulative and impulsive

Self mutilation – cutting
Splitting
Won’t remember negative behavior

High suicide rate **

329
Q

Histionic personality disorder

A

Excessive emotions
Attention seeking
Seductive behavior
Overly concerned with appearance – exaggerated

330
Q

Narcissistic personality disorder

A

Excessively preoccupied w/ personal prestige, power and vanity
Lack empathy
Require excessive admiration
React to criticism w/ rage

331
Q

Cluster C personality disorders

A

Anxiety, fearful, cowardly, compulsive, clingy

Avoidant
Obscessive compulsive
Dependent

332
Q

Avoidant personality disorder

A

Hypersensitivity to rejection
Socially inhibited and timid
Feelings of inadequacy
Desire relationships with others

333
Q

Obsessive compulsive personality disorder

A

Preoccupied w/ order, perfectionism and control

334
Q

Dependent personality disorder

A

Psychologically dependent on others
Low self esteem
Excessive need to be taken care of

335
Q

Membranoproliferative nephritis

A

Hep B, C
Lupus
RA
Monoclonal gamopathies

336
Q

Glomerulonephritis (GN)

A 
Light proteinuria
Hematuria
RBC casts
Azotemia (elevated BUN/Cr)
HTN
Oligouria
337
Q

Post-strep glomerulonephritis

A

Preceeded by Grp A strep – throat, impetigo
1-3 wks prior

Type III HSR – immune complexes deposit in glomeruli

Abx tx of strep does not prevent PSGN
-prevents acute rheumatic fever and heart disease

MC: kids
-borwn urine: “tea colored” “coca cola”

Renal bx: hypercellular glomeruli, N0

Dark “lumpy bumpy” subepithelial humps
-under foot process

Deposited in mesangium along BM:

  • IgG and IgM complexes
  • C3

activation of complement -> low C3
elevated ASO titer – may not elevate in impetigo

elevated anti-DNase B – in all infections

338
Q

Alport Sn

A

Type IV collagen – BM

Splitting of BM
Eye problems – cataracts, lenticonus
Nephritis
Deafness – high frequency hearing loss

“Can’t see, can’t pee, can’t hear high C”

339
Q

Rapidly progressive GN

A

-> RF fast

Cresentric GN: “crescendos”

  • cresent shaped deposits in glomeruli
  • fibrin, compliment, cell debris

Good pasture dz
Granulomatosis w/ polyangiitis
Microscopic polyangiitis
Lupus

340
Q

Good pastures dz

A

Type II HSR
Ab against BM
Linear Ab pattern – “fence pasture”
Pulmonary hemorrhage/hemoptysis

341
Q

Granulomatosis w/ polyangiitis

A

Lungs, kidney, upper airway – sinuses, hard palate

+cANCA – PR3-ANCA

342
Q

Microscopic polyangiitis

A

pANCA, MPO-ANCA

343
Q

IgA nephropathy – Berger dz

A

Assoc w/ Henoch-schonlein purpura

IgA immune complexes deposited in mesangium – dark, dense blobs in mesangium

Hematuria w/ RBC casts

Flares up after infection

344
Q

Henoch-Schonlein purpura

A 
Palpable purpura on buttocks and legs
Arthralgias
Abd pain
Intestinal hemorrhage
Renal dz – IgA nephropathy
345
Q

Diffuse proliferative glomerulonephritis

A

MC – severe form of lupus nephritis

Anti-dsDNA/DNA complexes deposit in subepithelium – between epithelium and BM

Line BM
Wire loop “wire lupus”

Can present as nephritic or nephrotic

346
Q

Nephrotic syndrome

A 
Proteinuria > 3.5 g/d
Hypoalbuminemia
Edema
Increased risk infection
Increased risk thrombosis
Hyperlipidemia
347
Q

Minimal change dz

A

Bx: flattening or effacement of podocyte foot processes
-> More permeability to protein

MC cause of nephrotic sn in kids

Triggered by infections/immunizations

Tx: corticosteroids

348
Q

Focal Segmental Glomerulosclerosis (FSGS)

A

AA and Latinos
HIV pts*

Bx: focal and segmental sclerosis – regions affected

349
Q

Membranous glomerulonephropathy

A

White adults

Bx:
Thickening of BM
Subepithelial immune deposits along BM

Domes and spikes**

350
Q

Membranoproliferative GN

A

Nephritic and nephrosis

“tram track” appearance – mesangium invades between “tracks”

IgG immune complex along BM
-subendothelial humps

Hep B, C, lupus, subacute bacterial endocarditis*

351
Q

Diabetic nephropathy

A

Microalbuminuria -> nephrotic sn
Thickening of GBM

Kimmelstiel – Wilson nodules
-round acellular nodules w/in glomeruli – pink

mesangium dramatically expanded

352
Q

Amyloidosis

A

Massive expansion of mesangial matrix
Amyloid protein deposits in mesangium

Congo red stain – apple green birefringence assoc w/ multiple myeloma

353
Q

APGAR

A

Appearance: cyanotic 0, acrocyanosis 1, pink 2

Pulse/HR absent 0, less than 100 1, over 100 2

Grimace no response to stimulation 0 cry, pull away 2

Activity/tone limp/floppy 0 flexed arms and legs, resists extension 2

Respiration no effort 0 slow irregular, labored 1 crying, vigorously breathin 2

354
Q

3 mo milestones

A

Gross motor: roll over

Fine motor: hands together

Verbal/Cognitive: laughing and squealing

Social/self-care

355
Q

6 mo milestones

A

Gross motor: sit up unassisted

Fine motor: transfer cube

Verbal/Cognitive: single syllables

Social/self-care self feed

Start of stranger anxiety

356
Q

9 mo milestones

A

Gross motor: crawling

Fine motor:

Verbal/Cognitive: object permanence

Social/self-care

Stranger anxiety

357
Q

12 mo milestones

A

Gross motor: stand, walk

Fine motor: block into cup

Verbal/Cognitive: 1-3 words

Social/self-care drink from cup

Stranger anxiety transitioning to separation anxiety

358
Q

15 mo milestones

A

Gross motor: walk backward, run

Fine motor: 2 cube tower

Verbal/Cognitive: 6 words

Social/self-care use utensils – fork, spoon

Separation anxiety

359
Q

18 mo milestones

A

Gross motor: climb stairs, kick a ball

Fine motor: 4 cube tower

Verbal/Cognitive: combine words

Social/self-care brush teeth w/ help

360
Q

2 y milestones

A

Gross motor: jump up

Fine motor: 6 cube tower

Verbal/Cognitive: half understandable

Social/self-care wash/dry hands

361
Q

3 y milestones

A

Gross motor: jump forward, ride tricycle

Fine motor: copy circle

Verbal/Cognitive: understandable

Social/self-care pour cereal, brush teeth, dress, play board games, potty training

362
Q

4 y milestones

A

Gross motor: hop on 1 foot

Fine motor: copy a plus sign

Verbal/Cognitive:

Social/self-care button clothes, magical thinking

363
Q

5 yo milestones

A

Gross motor: tie shoes

Fine motor: copy square and triangle

Verbal/Cognitive: identify colors, coins, count to five

Social/self-care

364
Q

6 yo milestone

A

Gross motor:

Fine motor:

Verbal/Cognitive:

Social/self-care – logical thinking “if…then…”

6-11 other sex is “yucky”

365
Q

Draw out steroid synthesis pathway

A

Page 639

366
Q

S/S of Cushing syndrome

A

“BAM CUSHINGOID”

Buffalo hump
Amenorrhea
Moon facies

Crazy
Ulcers
Skin changes – easy bruising, acne, purple striae, thin skin
HTN
Infection
Necrosis of femoral head
Glaucoma
Osteoporosis
Immunosuppression
Diabetes
367
Q

Embryonic origin and development of thyroid

A

Begins week 3

Derived from endoderm from floor of primitive pharynx

368
Q

Diabetes mellitus

A

Hyperglycemia -> polyuria, polydipsia, polyphagia, wt loss

Diagnostic tests:
Fasting serum glucose
2hr OGTT
Hemoglobin A1c

369
Q

Type 1 DM

A

Islet cells Ab against glutamic acid decarboxylase (GAD)

Primary insulin deficiency – younger onset

Assoc w/ HLA on CHr 6:
HLA-DR3 – DQ2
HLA-DR4 – DQ8

Acute complications: DKA

370
Q

Type 2 DM

A

Insulin resistance -> inadequate insulin production – burns out

Middle age or older

7/8 overweight or obese
very hereditary

other metabolic problems – high TG, cholesterol
HTN

Acanthosis nigricans on flexural areas

371
Q

Nonenzymatic glycation in DM

A

Glucose tacked onto:
Hemoglobin
Small blood vessels -> leaky

372
Q

Retinopathy of DM

A

Glycation of small vessels of retina

Nonproliferative
w/ new vessel formation -> proliferative
-fragil new vessels hemorrhage -> blindness

macular edema

cotton wool spots – not specific to DM

Need annual dilated eyes exam

373
Q

Diabetic nephropathy

A

Proteinuria
Progressive

Decreased by ACEI/ARBs

Kemmel Still-Wilson nodules – acellular nodules in glomerulus

374
Q

Diabetic vascular disease

A

Contributes to atherosclerosis -> coronary artery disease, stroke, PVD
-> dry gangrene -> amputations

375
Q

Diabetic neuropathy

A

Glucose –aldose reductase –> sorbitol –sorbitol dehydrogenase –> fructose

Insufficient sorbitol dehydrogenase in tissues, sorbitol levels elevated

  • schwann cells -> neuropathy
  • lens
  • retina
  • Kidney

Sorbitol pulls water into cell -> swelling and damage

376
Q

Motor, sensory, autonomic neuropathy in DM

A

Begins tips of toes, progresses proximally

Monofilament testing – can be asx early on

DM foot check – wounds, sensation

377
Q

DKA physiology

A

Profound insulin deficiency:
Cells can’t get any glucose -> production of ketones

Body stimulated to make glucagon – cells starving
-> elevation of blood glucose -> excessive polyuria and dehydration

-> breakdown fatty acids into ketones -> profound acidosis

378
Q

Precipitating factors for DKA

A

Absolute insulin deficiency:
Undx DM
Missed insulin dose

Stress body -> increased glucagon, catecholamines, cortisol:
Infection – pneumonia, gastroenteritis, UTI
Severe ischemic events – MI, CVA
Trauma
Dehydration
Alcohol and drug abuse (cocaine)

379
Q

Clinical features of DKA

A

Sx preceding acute illness

  • polyuria, polydipsia, wt loss
  • > dehydration

abd pain, N/V
confusion, delirium

sweet, fruity odor to breath

Kussmaul breathing – deep labored breathing, blowing off CO2

380
Q

DKA labs

A

Anion gap metabolic acidosis
Hyperglycemia of at least 250
Serum and urine ketones
Hyperkalemia – H/K ATPas exchanger pulls H+ into cell -> K+ out
-kidneys dump K+ -> total body K+ very low

381
Q

DKA complications

A

Arrhythmias – VT, torsades (low Mg)

Invasive fungal infecitons
-mucormuycosis, rhizopas -> invade sinuses -> brain abscess

382
Q

Tx of DKA

A

ICU

IV vluids
Insulin drip – stops ketone production, promotes glucose use

Monitor anion gap

  • insulin until gap closed, switch to IM
  • may need to coadminister w/ glucose

Potassium
May need Mg2+

383
Q

Hyperosmolar hyperglycemic state (HHS)

A

Primary presenting sx:
Confusion, delirium, coma

-> dehydration, N/V, abd pain

tx: IV fluids, insulin, potassium
monitor serum osmolarity

384
Q

DKA vs HHS

A

DKA:
Ketoacidosis – insulin absent
Hyperglycemia over 250
Anion gap

HHS:
No ketoacidosis – insulin present
Extreme hyperglycemia >800
Serum hyperosmolarity > 340
No anion gap
385
Q

Biguanides

A

Metformin

Decrease hepatic gluconeogenesis
Improves insulin sensitivyt

Does not cause wt gain

SE:
GI side effects common
Increased risk of lactic acidosis in renal failure

Caution w/ IV contrast – stop to prevent problems for a couple days

386
Q

Sulfonylureas

A

Glimepiride
Glipizide
Glyburide – more hypoglycemia

Stimulates continuous insulin release from beta cells
Close K channel in beta cell -> depolarizes, increased Ca2+ influx

SE:
Hypoglycemia – long lasting
Wt gain

Require pancreatic function

387
Q

Thiazolidinediones (TZDs)

A

“-glitazone”
Pioglitazone
Rosiglitazone

Improves insulin sensitivity
Decreases hepatic gluconeogenesis
Binds PPAR gamma receptor – adipose, sk.m., liver

SE:
Wt gain
Increased fluid retention -> increased risk of CHF
Possible hepatotoxicity

388
Q

DPP-4 inhibitors

A 
-gliptin
Sitagliptin
Alogliptin
Saxagliptin
Linagliptin

Inhibits DPP-4 which increases endogeneous GLP1 (inhibit the inhibitor)

  • > stimulation of insulin release, inhibit glucagon release -> lower blood glucose
  • ->delays gastric emptying

wt neutral

Low risk of side effects

389
Q

GLP1 agonists

A 
-glutide
Exenatide
Liraglutide
Albiglutide
Dulaglutide

Mimic incretin hormone GLP1

  • decreases glucagon
  • increases insulin secretion
  • delays gastric emptying (which reduces appetite)

effect glucose dependent

Wt loss

SE: nausea

390
Q

SGLT2 inhibitors

A

-flozin

Dapagliflozin
Empagliflozin
Canagliflozin

Inhibit Na+/glucose linked transporter in kidney -> glucose loss in urine

SE:
Risk w/ kidney dysfunction
UTIs, mycotic infections
Dehydration, polyuria
Possible DKA
391
Q

Metabolic syndrome diagnostic criteria

A

Any 3:

Abdominal obesity: over 40 in in men, over 35 in women

TGs over 150

HDL less than 40 in men, less than 50 in women

BP: over 130/85

Fasting serum glucose over 100 or 2 hr post OGTT over 140

392
Q

Warfarin

A

Inhibits epoxide reductase which recycles vit K

Increases PT

Used for chronic anticoagulation for afib, DVT prophylaxis and treatment, PE tx – prevents extension

Contra: pregnancy: bone/cartilage problems in epiphyses, nasal hypoplasia
-use heparin or LMWHs

393
Q

Platelet disorders

A

Microhemorrhages

  • bleeding from mucous membranes
  • epitaxi
  • petechiae – flat brown/red dots
  • purpura

increased bleeding time
normal PT/INR, PTT

394
Q

Immune thrombocytopenia (ITP)

A 
Chronic
Auto Ab (antiplatelet Ab) to GpIIb/IIIa on surface of platelets
-immune system destroys platelets
-> low platelets
high megakaryocytes on BM bx

Tx: steroids, IVIG, splenectomy – more platelets in circulation

395
Q

ADAMTS13

A

A disintegrin and metalloprotease w/ thrombospondin type I motif, number 13

Contains Zn

vWF multimers released from injured endothelial cells, ADAMTS13 cleaves multimers into smaller, active vWF units

396
Q

Thrombotic thrombocytopenic purpura

A

Excessive platelet activation -> widespread platelet thrombosis -> thrombocytopenia -> bleeding and purpura

Deficency of ADAMTS13 -> vWF multimers not broken down

Unregulated platelet aggregation -> widespread thrombosis
Consumption of platelets -> thrombocytopenia

Activation of coagulation cascade -> excessive fibrin mesh -> microangiopathic hemolytic anemia, schistocytes, elevated LDH

397
Q

Hemolytic uremic Sn (HUS)

A

Milder form of TTP

Kids – assoc w/ Ecoli O157:H7 infection

398
Q

Glanzmann Thrombasthenia

A

Genetic – chronic

Defect in glycoprotein IIb/IIIa -> abnormal platelet aggregation -> no plug

Normal platelet count

Increased bleeding time

399
Q

HUS vs TTP

A

HUS:
Hemolysis
Renal insuffiency (uremia)
Thrombocytopenia

TTP: HUS + fever and neurological sx (HA, confusion, seizures, coma, focal deficits like a stroke)

TTP: “FAT RN”
Fever
Anemia
Thrombocytopenia
Renal failure
Neurological sx
400
Q

Bernard-Soulier Sn

A

Genetic – chronic

Defect of GpIb -> platelet can’t bind to collagen -> defect of platelet plug formation

Platelet enlarged, removed form circulation -> moderate thrombocytopenia

Increased bleeding time (primary dysfunction)

401
Q

Von Willebrand Dz

A

Mixed platelet and coagulation disorder

MC inherited bleeding disorder
-defect of vWF

increased PTT (not stabilizing factor VIII)
Increased bleeding (platelets can’t adhere)

Dx:
vWF level
Factor VIII activity
Ristocetin cofactor assay –agglutinate RBC w/ vWF present: + if no agglutination

402
Q

Disseminated intravascular coagulation (DIC)

A

Acute, lifethreatening

Widespread activation of clotting ->

  • consumption of platelets and coagulation factors
  • hypocoagulable state -> bleeding

low platelets, elevated bleeding time
high PT/PTT
low fibrinogen, high fibrin split products (D-dimer)

Schistocytes on peripheral smear

Bleeding
Multiorgan failure

Causes:  “STOP Making Thrombi”
Sepsis (gram -)
Trauma
Obstetrics complications (amniotic fluid emboli, placental abruption)
Pancreatitis (acute)
Malignancy
Transfusion
403
Q

Small cell lung CA paraneoplastic effects

A

ACTH -> Cushing Sn

ADH -> SIADH ( low serum osmolality, hyponatremia -> seizures)

Lambert Eaton Sn

  • muscular weakness d/t Ab against presynaptic Ca2+ channels at NMJ
  • Test – isometric m. contraction – when let go able to contract m. strong d/t buildup of Ca2+
  • weakness improves w/ use

Cerebellar degeneration
-AutoAb attack purkinje cells in cerebellum -> dizziness and ataxia

404
Q

Squamous cell lung cancer paraneoplastic effects

A

Humoral hypercalcemia of malignancy

Tumor secretes PTHrP (like PTH)

  • > increased bone turnover, increased Ca2+ reabsorption in kidney
  • > elevated serum Ca2+
405
Q

Multiple myeloma paraneoplastic effects

A

Secretes local osteolytic factors -> lytic bone lesions -> hypercalcemia

406
Q

HL paraneoplastic effects

A

Secrete active vit D -> hypercalcemia

407
Q

PSA

A

Prostate CA

Any pathology increases PSA – BPH, prostatitis

408
Q

CA125

A

Ovarian CA

Anything irritation the peritoneum elevates CA125

409
Q

Alkaline phosphatase

A

Bone mets
Biliary dz
Paget dz of bone

410
Q

Alpha-fetoprotein

A

Hepatocellular carcinoma

Testicular tumor

411
Q

CA19-9

A

Pancreatic cancer

412
Q

CEA

A

Colon and pancreatic cancer

413
Q

S100

A

Melanoma
Schwannoma
-neural crest origin

414
Q

Tartrate resistant acid phosphatase (TRAP)

A

Hairy cell leukemia

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