Heme Flashcards

Question 1

Q

Anti- coagulants

Heparin: MOA; indication; HITT: what is it, sxs, tx; unfractionated: what does it do, measure; low molecular weight: significance, metabolism, other; administration
warfain: MOA, indication, advesrse affect

Answer

A

binds to anti-thrombin 3 and makes it work better -> inhibits factor 2, 9, 10, 11, 12; prevent DVT and PE; immune reaction against heparin that then atsrts acting on platelets and causes them to stick to eachother -> pt presents w/ clotting because -> use argatriban; inhibits factor 10 and 2 and causes more bleeding complications, PTT; smaller molecule that inhibits Factor 10a more than 2, so less bleeding complication, through kidney so need to monitor pts w/ renal dx, based on weight so hard to give to obese and pregnant pts bc need higher dose; given as injection on abdominal wall and with HITT reaction cause cause necrosis at injection site
atagonizes vit k -> onterferes with 2, 7, 9, 10, C and S; prevention of DVT; skin necrosis bc it depletes protein C -> bridge w/ hepain

Question 2

Q

Anti thrombotics

Aspirin: MOA; side effects;
Ticlopidine: MOA, indication, adverse effect
Clopidogrel: MOA, indication, adverse effect, dosage normally and after MI
Cilostazol: MOA, indication; side effect
Dipyridamole: MOA, indication, side effects

Answer

A

inhibits COX enzymes; at low doses it will inhibit only COX1 -> anti-thrombotic, at high doses it will inhibit COX 1 and 2 -> anti-thrombotic, analgesic, anti pyretic; GI ulcer -> bc of decrease in prostaglandin
irreversible blockage of platelet binding to fibrinogen, preventing activation of platelets; decrease stroke risk in those who cannot tolerate baby aspirin; increase risk of bleeding, neutropenia
Blocks platelet aggregation by inhibiting ADP receptor; decrease risk stroke, MI; bleeding and potential for hemorrhage (needs to be stopped before surgery); 75 mg 1x a day, but when placing stent give big dose during surgery because will immediately stop platelet adherence
inhibits phosphodiesterase 3 -> increase cAMP -> causes SM relaxation -> vasodilation; intermittent claudication and PAD; palpitation, headache
inhibits phosphodiesterase; w/ aspirin will decrease platelet life span and w/ warfarin will prevent emboli on artifical valves; will also increase adenosine which is potenet vasodilator -> exacerbates angina because will take blood away from some vessels that have calusdication and need higher and stronger flow.

Question 3

Q

Thrombolytics

streptokinase: indications; moa
urokinase: MOA
tissue plasminogen activator: indication; MOA
alteplase: indication; MOA

Answer

A

STEMI, only if dealing w/ ischemic tissue, also good for PE, DVT, and peripheral artery thrombosis; activated plasminogen into plasmin
same as streptokinase
reperfusion of occluded arteries; binds to fibrin and activates fibrin bound plasminogen into plasmin
acute MI, or stroke; MOA is same as TPA

Question 4

Q

GpIIb/IIIa Inhibitors

abciximab
ebtifibatibe
tirofiban

Answer

A

Fab of murine monoclonal antibody to human GpIIb/IIIa
cyclic peptide snake venom
non peptide antagonist

Question 5

Q

Hematopoeitic Drigs

erythropoeitin alpha: MOA, indications
filgrastrim: MOA, indications
sargramostim: indication, MOA
oprelvekin: MOA, indications

Answer

A

recombinant EPO; stimulates erythropoeisis; anemia w/ chronic renal failure
human recombinant granulocyte colony stimulating factor (stimulates production of PMN); when using myelosuppressive drugs
accelerates bone marrow replenishment when patient undergoes BM transplant; will stimulate all blood cell lines except for RBC and platelet
stimulates production of platelets; after chemo to increase platelet count

Question 6

Q

Erythrocyte Sedimentation Rate

what is it
stimulated by
high
low

Answer

A

non specific marker of inflammation
high levels of circulating fibrinogen
AI, CA, infection or pregnant
polycythemia, liver dx, sickle cell

Question 7

Q

Heme Synthesis

starts w
rate limiting enzyme
AA used
vitamin needed
Ferrochelatase
Ferrous vs ferric

Answer

A

Succinyl CoA
aminolevulinic acid synthase
glycine
B6
adds Fe2+ into porphyrin rings to make it heme; occurs in mito
ferrous (2+) bins to heme but ferric (3+) will not; ferric is what is absorbed in gut and is cannot be changed into ferrous bc of histidine

Question 8

Q

CO2 and Chloride Shift

- how is CO2 carrried

Answer

A

carbamate and bicarb; converted to bicarb in the RBC but then diffuses into plasma and Cl goes into the RBC

Question 9

Q

Types of anemia

iron deficiency: labs
sickle cell and thalassemia labs
lead poisoning and sideroblastic labs
chronic dx
AI hemolysis
hereditary spherocytosis
elliptocytosis
G6PDH def
Megaloblastic anemia

Answer

A

MCV lower than 80, ferritin is low
low MCV, normal ferritin, + Hb electrophoresis
low MCV, normal ferritin, - Hb electrophoresis
MCV 80-100; reticulocyte count normal
MCV 80-100; reticulocyte count normal

Question 10

Q

Types of anemia

iron deficiency: labs
sickle cell and thalassemia labs
lead poisoning and sideroblastic labs
chronic dx labs
AI hemolysis labs
hereditary spherocytosis and elliptocytosis labs
Megaloblastic anemia

Answer

A

MCV lower than 80, ferritin is low
low MCV, normal ferritin, + Hb electrophoresis
low MCV, normal ferritin, - Hb electrophoresis
MCV 80-100; reticulocyte count normal
MCV 80-100; reticulocyte count high, coombs test +
MCV 80-100; reticulocyte count high, coombs test -, Hb electrophoresis normal
MCV greater than 100, low B12 or folate

Question 11

Q

Iron deficiency anemia

iron and ferritin
TIBC
cause in children and young adults
cause in 20-40 yr old
cause in child bearing women
tx

Answer

A

decreased
increased
inadequate intake
ulcers and hemmorrhoids
period
ferrous sulfate 325 mg 2-3x a day

Question 12

Q

Sickle Cell anemia

caused by
type mutation
age
what happens
dactylitis
what causes anemia
crisis
vaso occlussive crisis
sxs
aplastic crisis
management: other
management: hydroxy urea
management: life time folic, why?
management: antibioitics, why?
management: cure
senicapoc: what is it, how does it work
avoid: hypoxic situations
protective against

Answer

A

qualitative problem bc valine is substituted for glutamic cid in beta chain
AR
6 mnths
hypoxia causes sickling -> vaso occlusion
fingers and toes experience RBC sickling leading to inflammation and extreme
hemolysis bc sickled RBC only last 10 days instead of 120 days
complications that occur bc of sickling
CVA, pulm infarction, splenic sequestration (can cause auto splenectomy), priapism (prolonged and painful erection)
exertional dyspnea, recurrent abd pain, bone pain
check reticulocyte and if it is not elevated then the patient is unable to make new RBC, usually caused by Parvo
oxygen, exchange transfusion
increase NO -> increase cGMP -> activates gamma globulin chain synthesis -> increase in HbF
lifetime folic -> bc constantly having to make reticulocytes bc of constant lysis of RBC
penicillen for meds
BM transplant
gardos channel blocker; usually allows K to leave RBC and water will follow causing dehydration of cell and leading to sickling; so we block channel
deep sea diving, airplane decompression, smoke inhalation, mountain climbing
malaria, infects and replicates in RBC; better to have sickle cell trait (hetero) because will have tolerance to infection but did not have sickle cell problems

Question 13

Q

Hemoglobin C dx

mutation
causes
sxs
sickling?
management

Answer

A

lysine replaces glutamic acid on b chain
leads to decrease in mobility
have mild hemolytic anemia, sporadic episodes of MS pain, bili rubin stones bc of hemolysis
blood cells do not sickle
eye exams (bc can have retinopathy)

Question 14

Q

Hemoglobin Electrophoresis

HbA vs HbS
HbA vs HbC

Answer

A

HbS replaced negative charged glutamic acid w/ non polar valine so HbS will not move as far down the electrode as normal HbA
HbC replaced negative charged glutamic acid w/ positively charged so HbC will not move as far down the electrode as normal HbA or HbS

Question 15

Q

Thalassemias

inhertiance
ethnicity
betha thal
alpha thal

Answer

A

AR, mutation produces defective mRNA
mediterranean
beta chain not produced correctly
alpha chain not produced correctly

Question 16

Q

Beta Thal

coded by
minor
major
thalssemia intermedia
tx of major

Answer

A

2 genes
asymptomatic; mild hypochromic microcytic anemia w/ increased HbF, A2 and target cells
both genes are missing; only see Hgb A2 and Hgb F on electrophoresis
mutation of kozak sequence, causing 30% decrease in production of beta chains
chronic transfusion, iron chelation, BM transplant

Question 17

Q

Alpha Thal

coded by
asymptomatic
2 genes missing sxs
3 genes missing sxs: Hgb Bart; Hgb H
alpha thal major: what is it, leads to, prognosis
tx for major

Answer

A

4 genes
1 gene missing
sxs only when active
sxs all the time; can produce Hgb Bart (hemogloin with 4 gamma chains) and has high affinity for O2 and will not deliver O2 to tissues; Hgb H is 4 beta chains and has high affinity for O2, no delivery to tissues
all 4 genes missing; cannot make hemoglobin; hydrops fatalis -> baby dies of HF
chronic blood transfusion, iron chelation (bc of blood transfusions), spleenectomy, BM transplant

Question 18

Q

Extramedullary Hematopoesis

what is it
description

Answer

A

liver and spleen help make RBC bc of chronic hemolytic anemia
enlargement of flat bones, skull or ribs

Question 19

Q

Blood Transfusions for thalassemia

given
1 unit of packed RBC increase
why packed RBC
rule of thumb
cyroprecipitate contains
transfusions reactions: anyphylaxis - what is it, sxs, management
transfusions reactions: febrile reaction - what is it, sxs, management
transfusions reactions: ABO reaction - what is it, sxs, management

Answer

A

when symptomatic
Hb by 1 and HcT by 3
only RBC, no plasma; whole blood is used for trauma
for every 2 units of pRBC, give 1 unit FFP (because diluting out all other blood products including clotting factors and will cause bleeding)
factor 8, vWF, and fibrinogen
caused by recipient not having IgA and blood products having IgA, causing recipients IgG to go off; flushing, swelling, wheezing; stop transfusion and give epi, next time filter blood for IgA
fever after transfusion bc of white cell antigens -> this is why cells are washed; give acetaminophen
RBC lysed, Fever and low back pain; stop transfusion, intubate, supportive care

Question 20

Q

Iron Overload

hemosiderosis
hemochromatosis: what is it, sxs, primary vs secondary,

Answer

A

deposition of hemosiderin in macrophages w/o tissue damage
iron overload in parenchymal tissue; restrictive cardiomyopathy, arthritis, testicular failure, discoloration of skin, joint and bone pain (psuedogout); auto recessive, chronic transfussion; phlebtomy and deferoxamine

Question 21

Q

Lead poisoning

what does it do
sxs
stored
sources
management: dimercaprol, EDTA, succimer

Answer

A

inhibit enzymes alpha aminolevulinic acid dehydratase and ferrochelatase -> cannot add iron to rings
basophilic stiffling -> porphyrin ring stuck to incise of RBC wall
abd pain and constipation, HA, lead line (blue pigmentation at gum and tooth lin), short term memory loss, loss appetite, irritability, depression
blood, soft tissue, bones
lead paint chips (taste sweet), chemical processing, spray pain, repairing radiators, miners
chelation: dimercaprol -> use in addition to EDTA bc can cross BBB; EDTA -> binds 2+ ions, give w/ calcium, does not cause BBB so does not help w/ encephalopathy, succimer -> water soluble, oral agent, recommended for children with lead level greater than 45

Question 22

Q

Anemia of Chronic dx

caused by
TIBC
ferritin
what happens
anemia of renal failure - cytokines and effect
chronic dx

Answer

A

chronic infectious or inflammatory process
decreased
increased
iron is stored in increased amount in marrow macrophages
IL beta, IL6, gamma IFN and TNF alpha -> inhibit EPO and erythroyte proliferation
macrophages begin to phago RBCs and increase in hepcidin to inhibit iron release

Question 23

Q

Coombs test

when is it done
direct: how
indirect: how, why?

Answer

A

MCV normal, reticulcyte count increased
antibodies are attached to antigen on RBC, so add coombs reagent which bind to antibodies on RBC and will cause RBC to agglutinate
pt will have antibodies in serum -> add reagent RBC, add combs reagent -> agglutination; used as prenatal or pre- blood transfusion test

Question 24

Q

AI hemo anemia

what is it
types
labs
cold
warm

Answer

A

premature RBC destruction that leads to anemia when BM cant keep up
intravascular (RBC lyse in circulation), extravascular (RBC phago by macrophages in liver or spleen)
reticulocytosis (BM trying to compensate), increased LDH, reduced plasma haptoglobin (protein bound to hb when loose in blood)
IgM mediated, only in cold temp, hemolysis through MAC
IgG mediated, body temp, causes opsonization and phago by macrophages

Question 25

Q

Hereditary Spherocytosis

- caused by

Answer

A

problem between ankyrin and spectrin

Question 26

Q

RBC shapes and meaning

Howell Jolly Bodies
Heinz body
Basophilic stippling
Tear drop cell
Target cell
Poikilocyte
schistocyte
burr cell
pappenheimer
cabots ring

Answer

A

nuclear remnant in RBC
G6PD deficiciency
porphyrin ring stuck inside RBC; lead poisoning
hemolytic anemia or CA
missing hb; thalassemia, and liver dx
cells in diff stages of development
fragmented RBC, mechanical cell
uremia
inclusion body w/ ferritin inside; sideroblastic and sickle cell
remnant of mitotic spindle; lead and pernicious anemia

Question 27

Q

Paroxsymal Nocturnal Hemoglobinuria

what is it
leads to
sxs
dx

Answer

A

acquired mutation of PIGA gene, coding for GPI anchor which normally protects RBC from complement
complement mediated RBC lysis
hemoglobinuria with dark urine throughout night
hams test -> check fragility of RBC when placed in acid

Question 28

Q

Macrocytic anemia

MCV
caused by
if RDW normal

Answer

A

over 100
B12 (has neuro sxs) or folate deficiency (no neuro sxs)
drugs, EtOH, liver disease

Question 29

Q

Thrombocytopenia

what is it
caused by
signs
most common causes
heparin induced throbocytopenia

Answer

A

low platelet count
elevated bleeding time (50K), dangerous bleeding (20k), bleeding into CNS (10K)
stem cell failure, splenic sequestration, increased destruction of platelets
idiopathic, thrombotic throbocytopenic purpura (lack of activity in the ADAMTS13 enzyme, VWF is not chopped up, platelets adhere easier, causes thrombosis), hemolytic, uremic sxs: caused by shigella toxin; DIC; drugs (heparin, sulfonamide, valproic acid)
pt produces antibodies against heparin which cross react with platelet factor 4 causes platelet destruction; as platelet count drops will get paradoxical thrombosis instead of bleeding; stop heparin and give direct thrombin inhibitor

Question 30

Q

Hypercoagulable Dx

Anti-thombrin 3 def
Protein C def
Protein S def
Factor V leiden
presentation

Answer

A

AD, decrease in anti-thrombin 3 -> thrombin cannot be inhibited
-
AD; abnrml factor V leiden cant be turned off
arterial and venous thrombosis

Question 31

Q

Growth of blood vessels

VEGF
FGF

Answer

A

stimulates angiogenesis

- promotes endothelial proliferation, migration and differentuation, important in hematopoesis and wound repair

Question 32

Q

Anatomy of artery

adventitia
tunica media
intima

Answer

A

contains vaso vasorum (blood supply to adventita and 2/3 media)
usually has elastin but under stress can produce collagen
supplied by blood through diffusion,

Question 33

Q

Arterioles

maintain
contain most
how
dilation
chronic hypertension
malignant hypertension

Answer

A

BP
SM by surface area
vasoconstrict and dilate
Beta 2 receptors
lead to reactive vasoconstriction -> hyaline arteriole sclerosis because increase in pressure causing damage to artery
hyperplastic arteriole sclerosis -> onion skinning

Question 34

Q

Capillaries

importance
continuous
fenestrated
sinusoidal
smooth muscle

Answer

A

gas and nutrient exchange
go straight into vein
endo cells have holes so more things can diffuse
gaps between cells so that bigger molecules can diffuse in and out
none

Question 35

Q

Vascular networks

parallel: type; resistance; calculation
series: examples, resistance, calculation

Answer

A

artery to capillaries to v; does not produce as much resistance; total resistance = 1 / (1/R1 + 1/R2 + 1/R3)
1 artery breaking into arterioles and then giving rise to capillaries, GI and hepatic circulation bc mesenteric v go into hepatic v; higher, total resistance = R1+ R2+ R3 +R4

Question 36

Q

Changes in diameter

small arteries
large vessels

Answer

A

changes in diameter and resistance of small a have greatest effect on vascular resistance bc make up 70% of total resistance in most organs
would have to compress by more than 50% in order to have significant effect on blood flow

Question 37

Q

Neuro Control of arterioles

under control of
how to dilate

Answer

A

sympathetics, constricted w/ alpha-1 (IP3/DAG)

- 90% of the time just turning down alpha 1 but can also use Beta 1

Question 38

Q

Types of pressure on inside of vessel

linear
transmural
what happens as vessel narrows

Answer

A

straight forward
pushing outward against vessel wall
velocity increases, flow decrease, resistance increases, BP increases

Question 39

Q

Capillary forces

hydrostatic high, oncotic low
hydrostatic = osmostic
hydrostatic low, oncotic high

Answer

A

on arterial side, hydrostatic is greater than osmotic -> fluid pushed out; oncotic pressure low because lots of fluid so not pulling
no movement
osmotic higher than hydrostatic so it is pushed back in; oncotic pressure high because not enough fluid and proteins attract positive charge of water

Question 40

Q

Transudate

what is it
how did it get out vasc
causes for hydro
causes for oncotic

Answer

A

mostly water
decreased oncotic pressure or increase hydrostatic pressure in vessel
kindey failure, and heart failure
kwashikor, cirrhosis, nephrotic syndrome (losing too much protein from kidneys), menientieres

Question 41

Q

Exudate

made up of
purulent
fibrinous
serous
malignant
catarrhal

Answer

A

protein and fluid
pus, live and dead tissue,
AI and rehumatic disorder
less protein, clear or slightly yellow… indicates inflammation or normal healing
has CA cells
found in nose and throat and has lots of mucus

Question 42

Q

Bilateral vs Unilateral LE edema

bilateral
unilateral

Answer

A

heart, kidney, liver failure

- vasc insuff, DVT

Question 43

Q

Ascites

what is it
type
SAAG: equation, high, low
gradient 1.2-2.5
gradient > 2.5
gradient <1.1

Answer

A

fluid accumulation in abd cavity
transudative or exudative
[protein] serum - [protein]
cirrhosis
heart failure or budd chiari
not due to increased hydrostatic pressure bs protein and fluis have same amount of protein -> nephrotic, TB or CA

Question 44

Q

Blood flow resistance

- equation

Answer

A

length times viscosity / diameter ^4

Question 45

Q

Arterio-nevous O2 diff

what is it
increases with
rest
exercise
after eating
studying
decreased

Answer

A

% O2 extracted by tissues
when tissue is metabolically active or decreased flow
heart
muscle
GI
brain
less metabolic activity, flow is increased or fistula

Question 46

Q

Fistula

congenital
caused
diseases

Answer

A

PDA
renal dialysis
von hippel lindau, osler weber

Question 47

Q

Anastamoses

what is it
importance
location

Answer

A

no capillaries, just goes straight from A to V
shunt blood away from non-essential structures at times of need
lips, ears, nose, finger/toes

Question 48

Q

Vericose Veins

why do they occur
smaller v
caused by
what happens when it can no longer accomodate
look like

Answer

A

valves do not function properly in larger v
spider v
DVT, pushed apart by increased standing
blood will leak out and cause skin to turn purple
dilated, tortous veins

Question 49

Q

Neuro Control of V

under control of
usually
constricted: how, why?

Answer

A

parasymapthetics
dilated
w/ alpha 1, only happens w/ blood loss

Question 50

Q

vasculitis

most common cause of death
sxs
wht happens
IgA nephropathies

Answer

A

heart failure, bc inflammation will attack hear vessels
petechiae, purpura, ecchymoses
PMNs comin, t cells and macophages follow at 4 days, fibroblasts come in at end to scar up
Berger and Henoch Schonlein

Question 51

Q

Vasculitis

Berger Dx (NO U): time frame, presentatoin, management
Buergers: what is it, associated w/, epi, sxs, raynauds phenomenon
Henoch- scholein purpura: sxs; epi; caused by; leukocytoclastic vasculitis
Diabetes
Syphylis
Kawasaki: type disorder, epi, size, hx of, acute sxs, sequalae/ aubacute sxs; mgmnt
temporal arteritis: epi, histo, sxs
polyarteritis nodosa: epi, size, associated with, pANCA, sxs
leukocytoclastic vasculitis: caused by, sxs

Answer

A

2 wks after common cold, present with hematuria, follow them and if get worse treat renal failure, if better just continue to watch
thromboangitis obliterans, strong, progressive and recurring inflammation and thrombosis of digital vessels; association w/ tobacco use; young, caucasian; gangrene; sensitivity to cold
raised rash (starts at waist and moves down), arthritis (ankles, knees, elbows), abd pain (GI hemmorrhage bc of intussusception); in child; antigen exposure causes IgA to be made and it implants in blood vessel wall and in renal mesangium; PMNs destroying blood vessel wall bc of IgA implantation
increased glucose causes increase viscocity -> increased inflammation AND excess glucose turns into sorbitol by enzyme aldol reductase which accumulates in nerves and causes neuropathy; symmetric, distal neuropathy (glove and stocking)
Leads to hyperplastic thickening of aortic walls -> oschemia to outer 2/3 of aorta -> aortic aneurysm
AI disorder; children; medium sized arteries; hx of viral infection; fever, myocarditis, conjunctivitis, strawberry tongue; coronary a aneurysm leading to MI, generalized desquamation rash; IV immunoglobulin, high dose aspirin, immunization for varicella and inflammation
older females; multi-nucleated giant cells adjacent to fragmented internal elastic lamina; headache, jaw pain, visual problems (steroids then biopsy)
middle aged men; fibrinoid necrosis of media of medium sized vessels; associated with hep B; pANCA neg; neuropathy, abd pain, melena, weight loss, malaise, fever
immun complex deposition because of drug allergy with neutrophil chemotaxis and damage -> give rise to palpable purpura

Question 52

Q

DIC

what is it
labs
management

Answer

A

activation of clotting cascade secondary to an insult (pancreatitis, gram - sepsis, burns) and burn through platelets so begin to bleed from everywhere
PT/ PTT elevated, elevated D-dimers
Fresh frozen plasma

Question 53

Q

Thrombotic Thrombocytopenia Purpura

what is it
sxs
managmenet

Answer

A

caused by aunto-antibody toward ADAMTS13, vWF not split, platelets start clotting
fever, anemia, thrombocytopenia, renal involvnement neuro sxs
plasmapharesis -> filter out antibodies and FFP

Question 54

Q

Ankylosing spondylitis

HLA
start w/
xray
- Schoerber test

Answer

A

B27
sacroiliitis
bamboo spine
aortitis -> lead to dissection, aortic regurg murmur

Question 55

Q

Collagen Vascular dx

CREST: what is it, sxs; antibody
Scleroderma: severe form of, histo, antibody
Progressive systemic sclerosis: what is it; antibody
Mixed CT disease: sxs, antibody

Answer

A

mildest form of scleoderma; calcinosis (dystrophic calcificiation), raynauds ( spasm of vessel of fingers and toes when cold -> give Ca channel blocker), esophageal dysmotility, sclerodactily: fingers and toes develop skin thickening; anti centromere antibody
more severe form of CREST , onion skining of kidney bc of HTN; anti-SCL 70 (anti-topo 1)
severe form of sclerosis that lead to scarring of liver and other organs, anti-SCL70
can have raynauds, arthralgia, sinusitis, esophegeal dysmotility; anti- ribnuclear protein antibody

Question 56

Q

Juvenile RA:

sxs
Oligoarticular
Systemic
Polyarticular
feltys disease
bechets

Answer

A

joint pain, joint swelling, fever;
1-4 months in first 6 months and 5 or fewer joints after first 6 months; higher incidence of ANA, non symmetrical
No limit to joint involvement, slamon pink rash and fever comes and goes with HSM
Involvement of 4 or more joints after 6 months w/ illness
RA + leukopenia + spleenomegaly
RA +G I/GU ulcers, erythema nodosa + PAD
RA + Xerophthalmia + Xerostomia

Question 57

Q

Schogrens

sxs
antibodies
diff from sicca syndroms

Answer

A

dry eye, dry mouth
anti-ro (SSA), anti-LA (SSB)
no arthritis and no antibodies

Question 58

Q

Serum Sickness

what is it
when
vaccine

Answer

A

measles like illness
2 weeks after vaccination
MMR

Question 59

Q

Subacute bacterial endocarditis

location
caused by
dx
tx

Answer

A

mitral valve
strep viridans
septic emboli (vegetation breaks off and end up in brain), roth spots on retina, splinter hemmorrhages, osler nodes (painful lesion on fingers and toes), janeway lesions (non-painful lesion on fingers and toes)
prophylaxis before dental surgery -> amoxicillin

Question 60

Q

Systemis Lupus Erythematosus

antibodies
anticardiolipin: what does it do; sxs; false positive on
dsDNA
COD
sxs
tx
renal dx, tramtrack appearance

Answer

A

snti-SMITH, anti-dsDNA, anti-cardiolipin
stimulates intrinsic clotting sxs; women with mult spontaneous abortions; VDRL when testing for syphilis
nephrotoxic w/o response to antibody
only vasculitis where most common cause of death is renal failure
malar rash
cyclophosphamide
membranproliferative glomerulonephritis; old basement membrane, complex deposited, new basement membrane (running parallel)

Question 61

Q

Cyro-globulinemia

what is it
when, mediated by
infections

Answer

A

antibody deposition affect any vessel in body
on ly with cold, igM
influenza, adenovirus, mycoplasma, hep B, EBV

Question 62

Q

Aneursym

what is it
cause by
risk
sites
fusiform vs saccular
true vs false/pseudo
sxs
abd aortic aneursym: sxs, rupture, increased risk of rupture, dx, tx, complications, screening
periphery
dissection: what is it; how?; all layers; presentation of aortic dissection; stanford A vs B; dx; tx

Answer

A

abnormal dilation of arter to more than 1.5 normal size
focal weakness in vessel wall
smoking
abd aorta, femoral, popliteal
sides get bigger vs sac pouching out of side
true is all 3 layers dilating vs false with only adventitia; caused by physician such as when removing needle -> pt starts bleeding and blood gets trapped by adventita layer
asymptomatic -> but rupture is painful/ uncomfortable
pulsatile abdominal mass, ruptures is surgical emergency bc large loss of blood; larger it is the greater the risk; US to confirm and get approx size, but CT or MRI when going to operate; only tx if greater than 5.5 cm because risk of rupture higher than risk from surgery; MI, renal failure, colonic ischemia, formation of fistula between aorta and duodenum; 65 y/o w/ hx of smoking
most common in popliteal a, bilaterally; many also have AAA
tear in an artery allowing blood to flow in the layers forcing them apart; brings up endo layer and gets into media layer splitting it into inner 2/3 and outer 1/3 then flows parallel under it; dissection through all 3 leas to blood loss; severe tearing pain originates in chest and radiates to scapula; proximal, involves ascending and arch -> need surgery, type B is descending -> managed with BP meds; get urgert x-ray (widening of mediastinum) or CT (visulaize false lumen); control BP with beta blocker, then if type A go to surgery but if type B then control BP chronically

Question 63

Q

Peripheral Vascular Dx

caused by
presents w/
dry gangrene: what is it; most common cause; management
wet gangrene: what is it; most common cause; management
leriche syndrome: what is it, sxs, dx, tx

Answer

A

atherosclerosis in LE
cramping like pain in LE after walking certain distance and pain is reproducible and consistent; shiny skin on LE w/o hair;
impaired blood flow to affected area w/ tissue discoloration, necrosis w/o infection, loss of limb; diabetes; does not need to be removed but recommend that it is
necrosis and infection; injury and not enough blood to heal; removal of limb, and leave open to make sure infection drains before it is closed up
aortoilliac insufficicency -> thigh and buttock claudication, diminished or absent femoral pulses, impotence; ABI (blood pressure at ankle/ blood pressure of arm) and duplex (triphasic -> normal, biphasic -> moderate, monophasic -> severe); lifestyle mods, cilastozol (PDE inhibitor) pentoxyfylline (causes RBC to traverse stenotic lesions easier), angioplasty

Question 64

Q

Vessel Dx

venous ulcer: caused by, location, sxs; tx
arterial: caused by, location, sxs; tx
carotid vascular dx: caused by
subclavian steal syndrome: what is it, caused by, sxs, dx, tx

Answer

A

incompetent valves leading to venous HTN; ankle/calf region; painless and shallow ulcer that contains granulation tissue in an attempt to heal; compression boots/stockings
secondary to occlusive artery dx; dorsum of foot, toes, heels; painful; bypass surgery
atherosclerotic plaque at carotid bifurcation; duplex; anticoagulation to prevent thrombosis and surgery if symptomatic with 50% or mor stenosis or asymptomatic with stenosis greater than 60%,
Occlusion of one of the subclavian a, uses other subclavian to supply brain and then takes blood supplied to brain to bring back to subclavain on other side of claudication; atherosclerosis, takayasu arteritis; presyncope, syncope, bad circulation in hands; CT, angiogram; stenet placement