Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
411 Cards in this Set
- Front
- Back
|
prevalence?
|
freq of patients w/ diseases within group
|
|
|
Incidence
|
# of new diseased pts within 1 year
|
|
|
calculation for sensitivity
|
TP/(TP + FN) x 100
|
|
|
calculation for specificity
|
TN/(TN + FP) x 100
|
|
|
calculation for PPV
|
TP/(TP+FP) x100
|
|
|
calculation for NPV
|
TN/(TN+FN) x100
|
|
|
what does a high BUN level indicate
|
Renal disease
poor renal perfusion excessive catabolism |
|
|
examples of poor renal perfusion that lead to high BUN levels
|
dehydration
shock GI bleeds |
|
|
examples of excessive catabolism that lead to high BUN levels
|
Burns
intense exercise diabetes fever |
|
|
causes of creatinine elevation
|
renal disease
muscle damage poor renal perfusion |
|
|
cause of prehepatic bilirubin elevation
|
hemolysis
|
|
|
cause of intrahepatic bilirubin elevation
|
liver disease
(hepatitis, cirrhosis) |
|
|
cause of post hepatic bilirubin elevation
|
Gall stones
|
|
|
cause of elevated alkaline phosphatase (ALP)
|
liver disease
bone disease pregnancy Leukemia's |
|
|
elevated to "significant" levels of LD in the blood indicate?
|
tissue damage
|
|
|
High levels of LD in the blood indicate
|
hemolysis
|
|
|
Where do you find AST in the body?
|
liver
cardiac muscle skeletal muscle |
|
|
Where do you find ALT in the body
|
Liver
|
|
|
what labs are used to diagnose MI's
|
CK-MB
Troponin I (&T) to a lesser extent LD myoglobin AST |
|
|
what labs are used to diagnose liver disease
|
AST/ALT
alkaline phosphatase LD gamma glutamyl transferase |
|
|
what labs are used to diagnose musculoskeletal diseases
|
CK, AST, LD, aldolase, myoglobin, ALP (in bone disease)
|
|
|
What are the causes of decreased prealbumin
|
malnutrition, alterations in liver function
|
|
|
What are the causes of increased prealbumin
|
dehydration
|
|
|
What are the causes of decreased albumin
|
impaired synthesis
increased loss |
|
|
what are the causes of impaired albumin synthesis
|
malnutrition, malabsorbtion, hepatic dysfunction
|
|
|
what are the causes of increased albumin loss
|
renal disease (nephritic syndrome), protein-losing gastroenteropathy, ascites
|
|
|
what is the major alpha 1 globulin?
|
a-1 antitrypsin
|
|
|
what does a-1 antitrypsin do
|
counters the effects of leukocyte esterase
|
|
|
when do you see an increase in a-1 antitrypsin
|
during inflammation
|
|
|
what are the pathologies associated with a-1 globulin deficiencies
|
COPD and emphysema
liver damage due to accumulation of misfolded proteins |
|
|
a-2 globulins
|
a-2 macroglobulin
haptoglobin CRP |
|
|
what are levels of CRP used for
|
indicator of tissue necrosis, acute infection, and inflammation, MI, Stroke
|
|
|
acute phase reactions/reactants
|
Neutrophilia
Thrombocytosis (platelets increase) Fibrinogen increased α -2-macroglubulin increased CRP increased Haptoglobin increased Albumin decreased ESR increased |
|
|
what is ESR used for?
|
indicator of inflammation
|
|
|
what accelerates ESR
|
Increased globulins, fibrinogen,
decreased albumin |
|
|
what are Gamma globulins and where do they come from?
|
antibodies from plasma cells
|
|
|
what would cause a decrease in gamma globulins
|
B-cell immunodefficiency
|
|
|
what are the 3 types of increased gamma globulin pathologies
|
polyclonal gammopathy
monoclonal gammopathy oligoclonal gammopathy |
|
|
what causes polyclonal gammopathy?
|
autoimmune diseases
chronic infections |
|
|
what causes monoclonal gammopathy
|
malignancy or premalignancy
|
|
|
exudate
|
high protein content
SG>3 WBCs |
|
|
lab results for an exudate
|
increase in LDH
|
|
|
causes of an exudate
|
infection
repair with angiogenisis |
|
|
Transudate
|
low protein
SG<3 |
|
|
causes of transudate
|
inc in hydrostatic pressure (heart failure)
decrease in osmotic pressure (liver and renal disease) lymph obstruction Na+ retention (renal disease) |
|
|
causes of local edema due to increased hydrostatic pressure
|
DVT or other obstruction
heart failure impaired venous outflow |
|
|
pathogenisis of increased hydrostatic pressure
|
Right sided heart fail
plasma volume expansion |
|
|
Molecular mediators of plasma volume expansion
|
renin
angiotensin aldosterone ADH |
|
|
what is a frequent initial manifestation of decreased colloid osmotic pressure?
|
periorbital edema
|
|
|
what are the causes of edema due to decreases colloid osmotic pressure
|
increased protein loss
decreased protein production water retention due activation of renin angiotensin sys |
|
|
lymphedema
|
Impaired lymphatic drainage leading to edema
|
|
|
what are the causes of lymphedema
|
trauma to lymphatic channels
removal of lymphatics radiation cancer metastases tumor compression infection of lymphatics |
|
|
what is dependant edema
|
impaired venous return
|
|
|
what are the causes of pulmonary edema
|
Left ventricular failure is most common
2-renal failure 3-Adult respiratory distress syndrome 4- pulmonary infections 5- hypersensitivity rxns. |
|
|
what is the morphology of pulmonary edema
|
lungs 2‐3x increase in weight
‐ frothy, blood tinged fluid ‐ hemosiderin‐laden macrophages in alveoli (Prussian blue stain positive cytoplasm) |
|
|
clinical features of pulmonary edema
|
SOB
rales tachpynea |
|
|
anasarca
|
severe generalized edema due to
end stage liver disease CHF shock |
|
|
associations with cerebral edema
|
Hypertensive crisis, encephalitis, trauma, hypernatremia.
|
|
|
morphology of cerebral edema
|
papilledema
Brain is swollen w/ flattened gyri and narrow sulci, |
|
|
serous effusion
|
yellow colored fluid
|
|
|
serosanguinous effusion
|
bloody effusion caused by
Trauma, malignancy or pulmonary infarction |
|
|
chylous effusion
|
a milky effusion caused by
Trauma, malignancy or pulmonary infarction |
|
|
Hyperemia
|
active arteriolar dilation
|
|
|
causes of hyperemia
|
exercise
inflammation (cyto, TNF) |
|
|
three examples of pathogenic hyperemia
|
erythema migrans
mastocytosis cellulitis |
|
|
what is congestion
|
impaired venous outflow
|
|
|
causes of congestion
|
heart failure
local venous obstruction |
|
|
characteristics of congestion
|
cyanosis
edema |
|
|
what is the mech of injury for congestion
|
hypoxia
hemorrhages siderophage accumulation |
|
|
cause of hepatic congestion
|
right sided heart failure
|
|
|
nutmeg liver
|
redish-brown liver due to right sided heart failure
centrilobular hemorrhagic necrosis |
|
|
what is congestive splenomegaly
|
passive congestion of the spleen
|
|
|
cause of congestive splenomegaly
|
Right sided heart failure
hepatic cirrhosis portal vein occlusion |
|
|
what is brown induration of the legs
|
venous insufficiency due to valvular defects
|
|
|
why the brown color in brown induration?
|
accumulation of siderophages
|
|
|
complications of brown induration?
|
stasis ulceration
|
|
|
what is hemostasis
|
blood that is fluid and free of clots
|
|
|
what are lines of zahn
|
a layered thrombus
|
|
|
hematoma
|
Mass of blood confined within an organ, tissue or confined space.
|
|
|
contusion
|
Bruise/ echymosis blunt force injury damages small BV’s w/o damaging tissue
|
|
|
ecchymosis
|
Large area greater than 1-2 cm of bruising
|
|
|
petechiae
|
Punctate hemorrhages associted w/ thrombocytopenia, dysfunctional plattlets and suffocation
|
|
|
purpura
|
Confluent petechiae > 3mm, similar cause as petichiae but include vascular inflamation and trauma.
|
|
|
hemarthrosis
|
Bleeding into a joint
|
|
|
laceration
|
Tear due to blunt force trauma, bridging strands are present
|
|
|
incision
|
cut made by sharp cutting object, clean margins w/o bridging
|
|
|
abrasion
|
Scrape in which superficial dermis is torn off by friction.
|
|
|
epistaxis
|
nose bleed
|
|
|
coughing up blood
|
hemoptysis
|
|
|
pooping blood
|
hematochezia
|
|
|
vomiting blood
|
hematemesis
|
|
|
melena
|
black blood in poop
|
|
|
hematuria
|
blood in pee
|
|
|
menorrhagia
|
excessive menstrual bleeding
|
|
|
key feature that clues you in to a laceration wound
|
bridging of blood vessels
|
|
|
5 steps of primary hemostasis
|
initial constriction then:
1. platelet adhesion (vWF & collagen) 2. shape change 3. Granule release (ADP,TXA) 4. recruitment 5. aggregation (plug formation) |
|
|
4 steps of secondary hemostasis
|
1.release of tissue factor from endo
2. phospholipid complex expression (platelets) 3. Thrombin activation 4. fibrin polymerization |
|
|
von wildebrand disease
|
defect in platelet adhesion
|
|
|
bernard-soulier synd
|
Gp1b deficiency
defect in platelet adhesion |
|
|
glansman thrombasthenia
|
defect in Gp11b111a
defect in platelet aggregation |
|
|
ADP receptor PY2 inhibitors
|
aggregation inhibitor
|
|
|
GP11b and GP111a inhibitors
|
blocks fibrin bridge
aggrigation inhibitor |
|
|
Aspirin / NSAIDS
|
COXs blockers
no TXA less aggregation |
|
|
Prostacyling PGI2
|
vasodialation
inhibition of aggregation |
|
|
NO
|
vasodilation
inhibition of platelet aggragation |
|
|
TXA
|
vasoconstrictor
stimulator of aggregation |
|
|
thrombocytopenia
|
reduced production of and increased destruction of platelets
|
|
|
what happens to platelets in cases of uremia
|
the become dysfunctional
|
|
|
thromboelastograph
|
used instead of bleeding time
|
|
|
platelet function analyzer
|
tests time to form a platelet plug
analogous to bleeding time |
|
|
bleeding time
|
used to test clot formation time
|
|
|
what is the reference range for platelets
|
150 - 350 x 10^3
|
|
|
Vit K dependent procoagulants
|
7
9 10 2 |
|
|
intrinsic coagulation cascade factors
|
8
9 11 12 |
|
|
extrinsic coagulation cascade factors
|
7
|
|
|
common coagulation cascade factors
|
10
5 2 |
|
|
tenase complex components
|
8 & 9a
|
|
|
go from tenase complex to thrombin activation
|
tenase activates 10
10 binds 5 = prothrombinase prothrombinase activates thrombin |
|
|
a PTT test tells you about which clotting factors?
|
intrinsic & common
|
|
|
a PT test tells you about which clotting factors
|
extrinsic & common
|
|
|
what is added to a PT test to make it work?
|
tissue factor
Ca++ phospholipid |
|
|
what is added to a PTT test to make it work
|
activating factor
Ca++ phospholipid |
|
|
what drug is the PT test designed to monitor
|
coumadin therapy
|
|
|
what drug is the PTT test designed to monitor
|
heparin
|
|
|
aquired coagulation factor diseases
|
liver failure
Vit K deficiencies anticoagulant drugs DIC |
|
|
hemophelia a
|
factor 8 deficiency
most serious |
|
|
hemophelia b
|
factor 9 deficiency
|
|
|
christmas disease
|
factor 9 deficiency
|
|
|
X linked deficiencies
|
factor 8
factor 9 |
|
|
what type of inheritance is vWF disease
|
autosomal dominant
|
|
|
vit K dependent anticoagulants
|
Protein C & S
|
|
|
what is the mode of action for Cumadin and warfarin
|
vit K antagonist
|
|
|
causes of vit K deficiencies
|
pancreatic disease
cystic fibrosis bile duct obstruction duodenum defects cumadin/warfarin therapy antibiotic therapy neonates |
|
|
what test is prolonged in Vit K deficiencies?
|
PT
if severe, PTT as well |
|
|
which test is prolonged in hemophilia A & B
|
PTT
|
|
|
thrombomodulin
|
binds thrombin
causes release of protein C & S proteolysis of 5 and 8 |
|
|
Antithrombin III + heparin
|
inactivate:
Thrombin 2 10 9 |
|
|
tPA
|
released by endothelial cells
activates Plasmin which lyses fibrin |
|
|
what is recombinant tPA used for
|
MI
Stroke Pulmonary embolism |
|
|
what deficiencies lead to thrombophilia
|
ATIII
Protein C & S |
|
|
PAI
|
blocks action of tPA
|
|
|
Virchows triad
|
pathogenic thrombosis factors
1. endothelial injury 2. stasis or turbulence of blood 3. blood hypercoagulability |
|
|
causes of abnormal blood flow (#2 in virchows triad)
|
atherosclerosis
aneurysms fibrillation hyperviscosity sickle cell |
|
|
Leiden mutation
|
mutated Va = resistant to Protein C proteolysis
Look for: caucasions reccurent DVTs |
|
|
prothrombin 20210A
|
mutation that leads to more prothrombin
3X risk of DVT |
|
|
hyperhomocystinemia
|
mutation of methyltetrahydrofolate reductase
inhibits ATIII & thrombomodulin Asians, caucasions, B-12 or folate deficiency |
|
|
high risk categories for secondary (aquired) hypercoagulability
|
smoking
bed rest MI a-fib tissue damage DIC cancer prosthetic heart valves over 60 c prior thrombosis hx obese sickle cell oral contraceptives |
|
|
HIT
|
heparin induced thrombocytopenia
Ab to heparin thrombus formation suspect if platelet count drops 50% |
|
|
antiphospholipid syndrome
|
Primary or secondary (lupus)
self reacting Ab Risk of recurrent: Stroke, MI, Pulm Emboli, DVT, miscarriage,libman sachs |
|
|
most common site for DVT?
|
Legs
|
|
|
most common effect of DVT dis-lodgement
|
Pulmonary embolism
|
|
|
clinical signs of DVT
|
50% asympt
edema Homans sign |
|
|
homans sign
|
pain in calf when dorsiflexed
|
|
|
diagnosis of DVT
|
abnormal D-dimer
ultrasound |
|
|
mural thrombus
|
forms in a chamber of the heart
systemic emboli |
|
|
chicken fat clots
|
clots formed postmortem
|
|
|
cor pulmonale
|
hypertrophy of Right Ventricle due to lung disease
|
|
|
side effect of angioplasty
|
atheroemboli
|
|
|
most common source of pulmonary emboli
|
deep veins of the leg
|
|
|
second most common source of pulmonary emboli
|
RV mural thrombus
|
|
|
fatal PEs are caused by?
|
saddle embolus
massive simultaneous emboli (>60% lung obstruction) |
|
|
most common arterial (systemic) emboli
|
intracardiac mural emboli (80%)
LV c MI LA c fib |
|
|
the other 20% of arterial emboli (less common)
|
aneurysm
atherosclerosis endocarditis paradoxical embolus |
|
|
paradoxical embolus
|
venous thrombus enters arterial sys via a R to L shunt in the heart
|
|
|
2 most common sites for arterial emboli
|
Legs- 75%
Brain- 10% |
|
|
Trousseau syndrome
|
chronic DIC due to pancreatic cancer
|
|
|
fat emboli
|
caused by trauma (usually long bones)
SOB, confusion, coma 1-3 days after fracture |
|
|
clinical setting for air embolus
|
obstetric procedures
treatment of pneumothorax |
|
|
amount of air needed to be clinically significant in air embolism
|
100cc or more
|
|
|
amniotic fluid embolism
|
gets in through a tear
clinical: SOB, shock, seziures, coma, DIC 80% fatality |
|
|
bland infarct
|
no infection
|
|
|
septic infarct
|
infected
|
|
|
red infarct
|
hemorrhagic
|
|
|
whit infarct
|
anemic
|
|
|
when do hemorrhagic (red) infarcts happen
|
venous or arterial occlusion in loose or previously congested tissue
|
|
|
when do white infarcts happen
|
in solid tissues
heart, spleen, kidney |
|
|
what endothelial component extracts triglycerides from VLDLs
|
lipoprotein lipase
|
|
|
what does niemann-pick type C disease do
|
fatty liver due to the inability of cholesterol to exit hepatocyte lysosomes
|
|
|
what does an accumulation of cholesterol in hepatocytes inhibit?
|
HMG CoA reductase (synth of choles)
LDL receptor synthesis |
|
|
what does an accumulation of cholesterol in hepatocytes activate?
|
ACAT (storage of cholesterol)
|
|
|
what are most cases of familial hypercholesterolemia caused by
|
LDL receptor defects
|
|
|
framingham index
|
10yr risk of MI
|
|
|
clinical features of hetero familial hypercholesterolemia
|
2-3x cholesterol levels
atherosclerosis |
|
|
clinical features of homozygous familial hypercholesterolemia
|
5-6x cholesterol levels
atherosclerosis xnthomas |
|
|
corneal arcus
|
lipid ring around the cornea
|
|
|
therapy for hypercholesterolemia
|
reduced fat intake
control blood sugar exercise Drugs: Statins (inhibit HMG-CoA reductase) Bile acid sequesterants (block resorption of cholesterol) Ezetimide (blocks absorption of cholesterol) Nicotinic acid |
|
|
ectasia
|
loss of vessel elasticity with age
|
|
|
what variables regulate normal blood pressure
|
CO and TPR
|
|
|
what is autoregulation
|
vasoconstriction in response to increased blood flow in vessel
|
|
|
essential HTN (primary)
|
idiopathic
-accounts for 90-95% of HTN |
|
|
secondary HTN
|
- most commonly secondary to renal disease
-5-10% of cases |
|
|
benign HTN
|
HTN at modest level and fairly stable over years
-95% of cases. |
|
|
malignant HTN
|
BP >200/120
if untreated, rapidly rising BP leads to death w/in 2yrs |
|
|
deffinition of hypertensive vascular disease
|
sustained BP > 139/89
|
|
|
hyaline arteriosclerosis
|
pink, hyaline thickening of arterial walls with a reduction in lumen size
common in diabetes |
|
|
hyperplastic arteriosclerosis
|
onionskin, concentric, laminated thickening of walls of arterioles with progressive narrowing lumen
|
|
|
what are the 3 varients of arteriosclerosis
|
athero
monckeybergs medial calcific arterio |
|
|
which varient of arteriosclerosis is most common?
|
Atherosclerosis
|
|
|
what are the constitutional risk factors for atherosclerosis
|
Age
male Family hx |
|
|
what are the modifiable risk factors for atherosclerosis
|
smoking
hyperlipidemia HTN diabetes CRP |
|
|
what is the response to injury hypothesis
|
the formation of fatty plaques due to damage of the endothelium
|
|
|
most common locations of atheroscleromas
|
lower abdominal aorta
coronary arteries popliteal arteries thoracic aorta internal carotids circle of willis |
|
|
what are the major consequences of atherosclerosis
|
MI
Stroke aortic aneurysms peripheral vascular disease |
|
|
preclinical phases of atherosclerosis
|
fatty streak
fibrofatty plaque advanced vulnerable plaque |
|
|
clinical phases of atherosclerosis
|
aneurysm and rupture
occlusion by thrombus critical stenosis |
|
|
true aneurysm
|
Bounded by complete (attenuated) arterial wall components
|
|
|
false aneurysm
|
Extravascular hematoma that communicates with intravascular space
|
|
|
what are the diseases that lead to aneurysm due to weak connective tissue in the vessel walls?
|
marfan
loeys-dietz ehelrs-danlos Vit C deficiency |
|
|
why does marfans lead to aneurysms
|
Defective synthesis of fibrillin (scaffolding) leading to abnormal TGF-B
and progressive weakening of Elastic Tissue |
|
|
why does loeys-dietz synd lead to aneurysms
|
Mutations in TGF-B receptors abnormalities of elastin, collagen I and
III |
|
|
why does ehelrs danlos synd lead to aneurysms
|
Defective Collagen Type III
|
|
|
why does Vit C deficiency lead to aneurysms
|
Altered Collagen Cross-linking
|
|
|
how does inflammation lead to aneurysms
|
increases amount of MMPs and decreases TIMPs
|
|
|
what are the 2 most common disorders that contribute to aneurysms
|
atherosclerosis
HTN |
|
|
What is a mycotic aneurysm?
|
Infection of a Major Artery that weakens the wall
|
|
|
what are the causes of mycotic aneurysms
|
- Septic embolus lodges in vessel
- Extension of adjacent infection - Circulating organisms directly infecting |
|
|
where do aneurysms associated with atherosclerosis usually occur
|
abdominal aorta
above bifurcation below renal aa. |
|
|
Who is more likely to get a AAA
|
- Men
- Smokers - 50 + |
|
|
What are the five clinical consequences of AAA’s?
|
-Rupture into peritoneal cavity
> Retroperitoneal tissue = potentially fatal damage - Impingement on adjacent structure - Occlusion of branch vessel > Downstream Ischemia - Embolism from atheroma or mural thrombus - Creation of abdominal mass (often palpably pulsating) |
|
|
At or above what size are AAA’s at greatest risk for rupture?
|
- >6cm (25% per year)
- >5cm surgically managed w/bypass grafts |
|
|
What are the clinical symptoms associated with a thoracic aortic aneurysm?
|
- Encroachment on mediastinal structures
- Respiratory difficulties (encroachment on the lungs) - Difficulty swallowing (compression of the esophagus) - Persistent cough (pressure on recurrent laryngeal nerve) - Pain (erosion of the bone) - Cardiac disease and Rupture |
|
|
What disease is a TAA associated with?
|
- Syphilitic (Luetic)
|
|
|
aortic dissection?
|
Dissection of blood vessel along the laminar planes of the aortic media, w/formation of a blood
filled channel w/in aortic wall |
|
|
What two groups of patients do dissections occur in?
|
- Men 40-60 years old (90% w/HTN)
- Patients w/abnormality of CT that affects the Aorta (Marfan Syndrome) |
|
|
What is the major predisposing factor for dissections?
|
HTN
|
|
|
What is the most frequent detectable microscopic lesion?
|
Cystic Medial Degeneration (preexisting lesion)
|
|
|
what are DeBakey type A dissections?
|
Proximal lesions, affect the ascending or ascending and descending
|
|
|
what are DeBakey type B dissections?
|
Distal lesions, beginning distal to Subclavian
|
|
|
What are the classical clinical symptoms for a dissection?
|
- Sudden onset of Excruciating pain, anterior chest, radiating to the back and moving downward
> Most often confused with Acute MI |
|
|
What is the most common cause of death with dissections?
|
Rupture of Dissection into any 3 major body cavities
|
|
|
What are the two most common mechanisms for vasculitis?
|
- Infectious Pathogens (direct invasions)
- Immune-Mediated Inflammation |
|
|
What are the common clinical findings in vasculitis?
|
- Fever, Myalgias, Athralgias, Malaise
- Tissue Ischemia |
|
|
What are the three main mechanisms which initiate noninfectious vasculitis?
|
- Immune Complex Disposistion (SLE)
- Anti-Neutrophil Cytoplasmic Antibodies - Anti-Endothelial Cell Antibodies |
|
|
What is an ANCA?
|
- Anti-Neutrophil Cytoplasmic Antibodies
|
|
|
What are the two types of ANCA?
|
- Anti-Meyeloperoxidase (MPO-ANCA) p-ANCA
- Anti-Proteinase-3 (PR3-ANCA) c-ANCA |
|
|
what are c-ANCAs associated with
|
Wegener Granulomatosis
|
|
|
what are p-ANCAs associated with?
|
Microscopic Polyangiitis & Churg-Strauss Syndrome
|
|
|
what vessels does Giant cell arteritis usually affect?
|
cranial vessels
|
|
|
What is the major morphologic finding of Giant cell arteritis
|
> Nodular intimal thickenings w/reduction of the lumen
> Granulomatous Inflammation (giant cells and fragmentation of the internal elastic lamina) |
|
|
What age group is Giant cell arteritis seen in?
|
>50
|
|
|
What are the symptoms of Giant cell arteritis?
|
- Insidious Presentation (fever, fatigue, weight loss)
-OR- - Sudden Onset of Headache, Tenderness w/Swelling and redness and facial pain - Ocular Symptoms (ophthalmic artery – why it must be treated) |
|
|
How is a definitive diagnosis of giant cell arteritis made?
|
- Biopsy (need 2-3cm length of vessel)
> Negative biopsy doesn’t rule out disease - Sed Rate and ESR both elevated |
|
|
What disease is giant cell arteritis commonly associated with?
|
polymyalgia rheumatica
|
|
|
treatment of giant cell arteritis
|
steroids
|
|
|
Takayasu arteritis affects what size vessel?
|
medium and larger arteries followed by fibrous thickening of aortic arch,
|
|
|
what is another name for takayasus disease
|
pulsless disease
|
|
|
What are the two main symptomsof takayasus disease?
|
- Marked weakening of Pulses
- Ocular Disturbances |
|
|
What are the major morphologic findings of takayasu arteritis?
|
- Involvement of Aortic Arch (pulseless disease)
- Irregular thickening of vessel wall with intima hyperplasia - Mononuclear inflammation, Granulomatous inflammation, then Collagenous Fibrosis |
|
|
what age group does takayasu arteritis usually affect
|
<50yrs
|
|
|
What is the course of Takayasu's disease?
|
Fatigue, weight loss and fever
Progresses to Vascular symptoms - Weaker pulses in upper extremity - Cold or numb fingers - Ocular Disturbances - Neurologic Deficits - Course is variable, rapid progression or quiescent stage after 1-2 years |
|
|
what is PAN?
|
polyarteritis nodosa
|
|
|
PAN affects what size vessels?
|
Necrotizing inflammation of small or medium sized muscular arteries
|
|
|
PAN affects renal and visceral vessels, what does it spare?
|
- Pulmonary vessels
|
|
|
What are the morphologic features of PAN?
|
- Segmental Transmural Necrotizing Inflammation
> Acute – Fibroid necrosis, neutrophils, eosinophils, mononuclear cells > Healing – Transmural Scarring, continuing necrosis > Healed – Fibrotic Thickening |
|
|
Do patients get glomerulonephritis from PAN?
|
No, small vessels are spared
|
|
|
what age group does PAN affect?
|
young adults
|
|
|
Natural course of PAN with/without treatment?
|
with- 90% remission
Without- fatal |
|
|
What is treatment for PAN?
|
- Corticosteroids and Cyclophosphamide
|
|
|
What are the three features of Churg-Strauss syndrome?
|
- Asthma
- Allergic Rhinitis - Peripheral Eosinophilia |
|
|
What other vasculitis has the same characteristic lesion as Churg-Strauss?
|
PAN
|
|
|
What is the other name for Kawasaki disease?
|
- Mucocutaneous Lymph Node Syndrome
|
|
|
what is the leading cause of aquired heart disease in children
|
Kawasaki's disease
|
|
|
What arteries does Kawasaki's involve?
|
coronary aa.
|
|
|
What are the symptoms of mucocutaneous lymph node syndrome?
|
- Fever
- Conjunctival and Oral Erythema and Erosion - Edema of the hands and feet - Erythema of palms and soles (later desquamation) - Cervical Lymphadenopathy |
|
|
Patients with MLNS develop what complications? (Kawasaki's)
|
> Untreated (20%) -->Cardiovascular Sequelae
> Treated (4%) w/IV immunoglobulin and Aspirin ---> coronary Artery Disease |
|
|
What are the morphologic features of Kawasaki's?
|
- Transmural Necrosis Inflammation (like PAN, but not as severe)
|
|
|
What size vessels are affected in microscopic polyangiitis?
|
small vessels
|
|
|
what is the fatality % for kawasaki's
|
1-2%
|
|
|
How does microscopic polyangitis present?
|
Palpable purpura involving skin, mucous membranes, brain, lungs, GI, muscles,Heart, Kidneys
|
|
|
Major clinical features of microscopic polyangitis?
|
- Hemoptysis
- Hematuria - Bowel Pain -Proteinuria - Arthragias - Muscle Pain/Weakness - Hemorrhage |
|
|
How is a definitive diagnosis of microscopic polyangitis made?
|
- Skin Biopsy (often diagnostic)
- p-ANCA (MPO – ANCA’s) seen in 70% |
|
|
What two features distinguish microscopic polyangitis from PAN?
|
- Necrotizing Glomerulonephritis
- Pulmonary Capillaritis |
|
|
Morphologic features of microscopic polyangitis?
|
> Segmental Fibrinoid Necrosis
-OR- > Leukocytoclasia |
|
|
What is the triad that characterizes Wegener Granulomatosis?
|
1 – Acute Necrotizing Granulomas of upper and/or Lower Respiratory Tracts
2 – Necrotizing –OR- Granulomatous Vasculitis of Small to Medium Size Vessels > Mostly in the Lung and Upper Airway (can have other sites though) 3 – Renal Disease |
|
|
Major morphologic features of Wegeners disease?
|
> Upper Respiratory Tract
- Inflammatory Sinusitis (mucosal granulomas) - Ulcerative lesions of Nose, Pharynx or Palate > Necrotizing granulomas and necrotizing or granulomatous vasculitis > Renal Lesions - Focal Necrotizing, often Crescentic, Glomerulonephritis |
|
|
What sex and age does Wegener's disease affect?
|
Males>females
ave- 40 yrs |
|
|
Clinical features of Wegener's?
|
- Pneumonitis (lung) w/bilateral nodular and cavitary infiltrates
- Chronic Sinusitis and Ulceration of Nasopharynx (URT) - Evidence of Renal Disease |
|
|
Natural course of Wegeners's disease?
|
- Untreated --> 80% Die within 1 year
- Treated (Steroids, Cyclophosphamide and TNF-antagonists) -->Chronic relapsing / Remitting Disease |
|
|
What is the other name for thromboangiitis obliterans?
|
buergers disease
|
|
|
What group of people get thromboangiitis obliterans?
|
- Heavy Cigarette Smokers (predominantly male, before age 35)
|
|
|
Morphologic features of thromboangiitis obliterans?
|
- Acute and Chronic Inflammation w/Luminal Thrombosis
- Microabscesses w/in Thrombus, Wall of Granulomatous Inflammation |
|
|
What is Raynaud phenomenon?
|
- Exaggerated Vasoconstriction of digital arteries and arterioles
|
|
|
Clinical features of reynauds?
|
Paroxysmal pallor or Cyanosis of the digits of the hands and feet
|
|
|
who gets primary reynauds
|
young females
|
|
|
What is secondary Raynaud’s?
|
Vascular Insufficiency of the Extremities, secondary to arterial narrowing from various processes:
> SLE > Scleroderma > Atherosclerosis > Buerger Disease |
|
|
What veins account for majority of cases of thrombophlebitis and phlebothrombosis?
|
90% are deep veins
|
|
|
The superior vena caval syndrome is cause by what?
|
- Neoplasms that compress or invade superior vena cava
> Primary Bronchogenic Carcinoma > Mediastinal Lymphoma |
|
|
Clinical features of superior vena cava syndrome?
|
- Dusky Cyanosis
- Marked Dialation of the Veins in the Head, Neck and Arms |
|
|
The inferior vena caval syndrome is caused by what?
|
Neoplasms that compress or penetrate the walls of the vena cava or thrombus that may propagate upwards
> Hepatocellular Carcinoma > Renal Carcinoma |
|
|
Clinical features of IVC syndrome?
|
- Marked Leg Edema
- Distension of Superficial veins of the Lower Abdomen - Massive Proteinuria (involvement of the renal veins) |
|
|
When does systolic dysfunction occur?
|
ischemic injury, pressure/volume overload, dilated cadiomyopathy
|
|
|
when does diastolic dysfunction occur
|
massive LV hypertrophy, myocardial fibrosis, deposition of amyloid, constrictive pericarditis
|
|
|
What three mechanisms does the cardiovascular system use to maintain pressure and perfusion in the face of damage or excess burden?
|
-frank-starling
-myocardial hypertrophy with/without cardiac chamber dilation -activation of neurohumoral systems |
|
|
What two features characterize CHF?
|
-diminished cardiac output-forward failure
-damming back of blood-backward failure |
|
|
What are the three most common underlying disease states for CHF? (Account for 90%)
|
-Hypertension
-MyocardIal infarction -diabetes mellitus |
|
|
What are the two patterns of hypertrophy in the heart?
|
-Concentric hypertrophy-occurs with pressure overload ventricles
-Dilation-occurs with volume overloaded ventricles. |
|
|
What four morphologic features are seen in CHF?
|
-increased heart weight
-progressive wall thinning -chamber dilation -microscopic change of hypertrophy |
|
|
. What are the four most common causes of left sided failure?
|
-Ischemic heart disease
-hypertension -Aortic and mitral valvular disease -nonischemic myocardial diseases |
|
|
What happens to the left atrium in left heart failure?
|
-It enlarges and causes atrial fibrillation.
|
|
|
What three changes occur in the lungs with left heart failure?
|
-Perivascular and interstitial transudate
-edematous widening of alveolar septa -accumulation of edema fluid in alveolar spaces |
|
|
What are heart failure cells ?
|
-hemoisderin containing macrophages in alveoli
|
|
|
What are possible clinical manifestations of the lung changes in Left sided heart failure?
|
-Dyspnea
-Orthopnea-dyspnea on lying down, relieved by sitting/standing -Paroxysmal nocturnal dyspnea-attacks of extreme dyspmea bordering on suffocation -cough |
|
|
What is the most common cause of right heart failure?
|
-left sided failure
|
|
|
Pure right sided failure occurs with what?
|
-Chronic severe pulmonary hypertension and is called cor pulmonale.
|
|
|
What four changes occur in the liver with right sided heart failure?
|
-Nutmeg liver-chronic passive congestion congested red centers of liver lobules surrounded by paler peripheral regions
-Centrilobular necrosis -Central hemorrhagic necrosis-severe, rapidly developing failure leads to rupture of sinusoids -cardiac sclerosis-long standing severe failure, central areas become fibrotic |
|
|
What happens to the spleen in right sided heart failure?
|
-Spenic congestion- enlarged, firm spleen, may weigh 500-600g. Fibrous thickening of sinusoidal walls=congestive splenomegaly
|
|
|
What is ascites?
|
-transudate in peritoneal cavity
|
|
|
What is anasarca?
|
extreme generalized edeema. Especially in ankle.
|
|
|
What five categories of heart disease account for almost all cardiac mortality?
|
-Ischemic heart disease
-hypertensive heart disease and pulmonary hypertensive heart disease -certain valvular disease -congenital heart disease |
|
|
Which category of heart disease accounts for 80-90% of deaths
|
ischemic injury
|
|
|
In 90% or more of cases what is the underlying cause of myocardial ischemia?
|
-coronary artery obstruction
|
|
|
What is another name for IHD? (ischemic heart disease)
|
-Coronary artery disease
|
|
|
What four syndromes describe the clinical manifestations of IHD? (ischemic heart disease)
|
-angina pectoris
-myocardial infarction -chronic ischemic heart disease -sudden cardiac death |
|
|
What two things have led to a decrease in death due to IHD?
|
-prevention by change in lifestyle
-diagnosis and therapeutic advances |
|
|
What is acute plaque change?
|
-plaque that develops in the first 2cm of the LAD and LC and distal thirds of RC
|
|
|
What are the acute coronary syndromes?
|
-Unstable angina
-acute MI -Sudden cardiac death |
|
|
what are the symptoms and underlying causes of stable angina?
|
reduction of coronary perfusion to a critical level by chronic stenosing atherosclerosis
|
|
|
what are the symptoms and underlying causes of printzmetals angina? (also called varient)
|
angina that occurs at rest. Due to coronary artery spasm. Elevation of ST segment on EKG.
|
|
|
what are the symptoms and underlying causes of unstable angina? (also called crescendo)
|
Pain gets worse and lasts longer. Induced by fissuring, ulceration or rupture of plaque with superimposed (partial) thrombus and possibly embolization. Often prodrome of MI=preinfarction angina
|
|
|
What are the two types of MI?
|
transmural
subendocardial |
|
|
what is a transmural MI?
|
ischemic necrosis involves the full thickness of ventricular wall
|
|
|
what is a subendothelial MI?
|
ischemic necrosis limited to the inner one-third or at most one half of the ventricular wall, extends laterally beyond perfusion area of single artery
|
|
|
Which sex is protected from MI until middle age?
|
-females
|
|
|
What three possible events, unrelated to atherosclerosis, occur causing an MI?
|
-vasospasm +/- atherosclerosis may cause deficit
-emboli from left mural thrombosis, vegatative endocarditis, paradoxic emboli from right -unexplained-no atherosclerosis |
|
|
What seven things account for the location, size and morpoholgic features of an MI?
|
-location, severity, and rate of development of coronary occlusion
-size of vascular bed perfused by vessel -duration of occlusion -metabolic/oxygen needs of at risk myocardium -extent of collaterals -presence site and severity of coronary artery spasm -alterations in blood pressure, heart rate and cardiac rhythm |
|
|
******Describe the sequence of events grossly and microscopically for an MI *********
|
-Gross features: after2-3 hours can highlight necrosis with histochemical method-triphenyltetrazolium (TTC). Colors noninfarct area red. infarct pale
-Morphologic: coagulation necrosis and inflammation. Formation of granulation tissue. Resorption of necrotic myocardium. Organization of granulation tissue from scar. |
|
|
How may reperfusion to an infarct occur?
|
-Restore coronary blood flow by thrombolysis, baloon angioplasty, or coronary arterial bypass graft.
|
|
|
What two laboratory measurements are useful to diagnose an acute MI?
|
CK-MB and Troponin
|
|
|
What four factors are associated with a poor prognosis after MI?
|
1)Diabetes
2)Being female 3) Old age 4) Previous MI |
|
|
what are the 3 types of cardiac rupture syndromes, post MI
|
1.Rupture of ventrivular free wall--> hemopericardium and tamponade--> death **Most common rupture** Rupture occurs 3-7 days post MI
2. Rupture of septum--> L to R shunt 3. Papillary muscle rupture--> **acute mitral regurgitation** |
|
|
What three things determine complications and prognosis after an MI?
|
1. Infarct Size
2. Infarct Site 3. Transmural Extent |
|
|
Chronic ischemic heart disease is usually due to?
|
by ischemic damage that resulted in CHF--> post infarction there is cardiac decomposition (the heart has been damaged many times)
|
|
|
Sudden cardiac death is defined as?
|
an unexpected death that results from cardiac causes within 1 hr with or without the onset of symptoms.
|
|
|
The majority of sudden cardiac death cases in adults are due to
|
lethal arrhythmia, or atherosclerosis. 80-90%
|
|
|
What are the minimal criteria for diagnosing systemic hypertensive heart disease?
|
1) LV hypertrophy (concentric) in absence of other causative pathology
2) History or pathologic evidence of HTN |
|
|
what is the gross morphology of systemic hypertensive heart disease
|
1) LV pressure overload LV circumferential hypertrophy w/o dilation
2) Symmetric wall thickening (↑2cm) 3) Increased heart weight (↑500g) 4) Stiff heart impairs diastolic filling 5) Decomposition occurs with dilation, thinning of wall producing an enlarged heart |
|
|
What are the two types of cor pulmonale?
|
1) Acute -->RV dilation due to massive pulmonary embolism
2) Chronic -->RV hypertrophy and later dilation secondary to prolonged pressure overload from pulmonary artery obstruction |
|
|
What are the four groups of disorders predisposing to cor pulmonale
|
Diseases of the:
pulmonary parenchyma pulmonary vessels chest M.S. functioning pulmonary arterial functioning |
|
|
what are the 3 main, predisposing factors for cor pulmonale
|
1) Chronic bronchitis
2) Emphysema 3) COPD |
|
|
main cause of mitral stenosis
|
rheumatic fever
|
|
|
main cause of mitral regurg (insufficiency)
|
MVP
(Myxomatous degeneration) |
|
|
main cause of aortic stenosis
|
calcification
|
|
|
main cause of aortic insufficiency (regurg)
|
aortic dilation (related to HTN and age)
|
|
|
What are the three most common calcific valvular diseases?
|
1) Aortic stenosis
2) Mitral annular calcification 3) Mitral valve prolapsed |
|
|
What are the two types of calcific aortic stenosis?
|
1) Senile calcific aortic stenosis --> **most common***Mostly age related (70-80 yrs old)
2) Congenitally bicuspid aortic valve --> 1-2% of the population have this |
|
|
What is the major difference between the calcification of a congenitally bicuspid valve and a normal aortic valve?
|
the 2 cusps are of unequal size, the larger cusp has no midline raphe; predisposed to progressive calcification
|
|
|
What is the anatomic change in the heart associated with mitral valve prolapse?
|
Ballooning of mitral leaflets which are often thick
and rubbery |
|
|
Which sex is more likely to get MVP?
|
more common in young women
|
|
|
what are the possible complications of MVP
|
1) Infective endocarditis
2) Mitral insufficiency 3) Stroke (systemic infarct from thrombi that accumulate on valve) 4) Arrhythmias |
|
|
what are the clinical features of MVP
|
1) Asymptomatic --> discovered on routine exam as mid-systolic click
2) murmur and click 3) Echocardiography is diagnostic |
|
|
what are the major manifestations of RF within the jones criteria
|
1)Migratory polyarthritis of large joints
2)Carditis 3)Subcutaneous nodules 4) Erythema of skin 5) Sydenham’s chorea (neurologic disorder) |
|
|
what are the jones criteria of minor RF manifestations
|
1. fever
2. arthralgias 3. acute phase reactants |
|
|
what are the requirements to meet the jones critera for RF
|
Evidence of GABHS &:
- 2 major manifestations OR - 1 Major & 2 minor manifestations |
|
|
What are the 3 key pathologic features for acute RHD
|
1.vegitations on mitral valve leaflet
2. ashcroff bodies in the myocardium 3. fibrinous pericarditis |
|
|
Chronic RHD presents as
|
mitral stenosis
|
|
|
what is the standard practice for individuals that have been diagnosed with RF?
|
prophylactic antibiotics long term
|
|
|
what is infective endocarditis and what are the two types?
|
Infection, invasion or coloniztion of the heart by a microbe
types= acute and subacute bacterial endocarditis |
|
|
infection source of endocarditis
|
‐ Infection elsewhere‐ abscess, dental caries
‐ UTI (urinary tract infection) ‐ Dental/surgical procedure ‐ IV drug use: contaminated needles ‐ Occult source in GI tract ‐ Trivial breaks in skin |
|
|
factors that predispose you to endocarditis
|
anomalous valves (malformed)
artificial valves immunodeficiency diabetes Drug and alcohol abuse |
|
|
acute endocarditis
|
rapid progression
new murmur (vegitations) embolizations mortality of 30% |
|
|
subacute endocarditis
|
weeks to months
petechiae structural cardiac disease develops slowl fatal if not aggressively treated |
|
|
what is the most common cause of acute endocarditis and who is most at risk for it
|
S. aureus (high virulence)
IV drug users |
|
|
what is the cause of subacute endocarditis
|
Low virulence organisms:
Strep. veridans Strep. bovis S. epidermidis |
|
|
what are the systemic complications of infective endocarditis
|
1- Cerebral stroke and retinal emboli
2- Mycotic aneuysm 3-Valve complications/myocardial abcess 4-Spleneomegaly 5- Pneumonia/ infarction 6- Renal infarct/ abcess/ glomerulonephritis 7- Splinter hemorrhages/ janeway lesions 8- clubbing 9- Anemia of chronic dis. Osteomyletis 10- Hematuria |
|
|
morphology of infective endocarditis
|
Vegetations on heart valves
Friable and bulky |
|
|
most common valves affected by Infective endocarditis
|
mitral and aortic
Tricuspid in 50% of IV drug users |
|
|
cardiac complications of infective endocarditis
|
heart failure
valvular disease ring abscess (valve perforation) artificial valve dehesience supuritive pericarditis |
|
|
NBTE?
|
nonbacterial thrombotic endocarditis
sterile deposits on valves associated with cancer (trousseau synd) |
|
|
What are the associations and consequences of Libman-Sacks endocarditis?
|
Autoimmunity of SLE and antiphospholipid syndrome
|
|
|
cause of carcinoid heart disease and Lab test for it
|
carcinoid tumors
5-HIAA |
|
|
morphology of carcinoid heart disease
|
thickening of
RV Tricuspid pulmonic |
|
|
complications with artificial valves
|
Thromboembolic disease
Infective Endocarditis (S. epi) structural deterioration (in bio valves. calcify, tear) hemolytic anemia fibrosis of valve leaky |
|
|
what type of dysfunction is dilated cardiomyopathy?
|
systolic dys
|
|
|
what type of dysfunction is hypertrophic cardiomyopathy?
|
diastolic dys
|
|
|
what type of dysfunction is restrictive cardiomyopathy?
|
diastolic dys
|
|
|
morphology and characteristics of dilated cardiomyopathy?
|
-idopathic (c lots of predisposing factors)
-globular, enlarged, heavy LV -mitral regurg because of dilation of LV -mural thrombi common -myocyte hypertrophy -fibrosis - EF <25% |
|
|
morphology and characteristics of arrythmogenic RV cardiomyopathy
|
RV enlargement
wall is severely thin, fatty, fibrotic |
|
|
morphology and characteristics of hypertrophic cardiomyopathy
|
100% genetic
massive hypertrophy esp IVS reduced chamber size and SV dynamic obstruction to outflow a-fib with mural thrombus formation sudden death in athletes |
|
|
morphology and characteristic of restrictive cardiomyopathy
|
-decreased compliance of LV
-dilated atria -amyloidosis (transthyratin) -older individuals |
|
|
morphology of myocarditis
|
viral = lymphocytes.
hypersensitivity = eosinophils & Macs chaga = myofiber distnesion with trypanosomes |
|
|
causes of myocarditis
|
-lyme disease (5%)
-diptheriae -trichinosis -toxoplasmosis, chagas disease |
|
|
what is Chagas disease
|
Trypanisoma cruzii
|
|
|
pathology of iron overload on the heart
|
Dilated heart with Prussian blue stain.
|
|
|
pathology of the heart with hyperthyroidism
|
myocardial hypertrophy
|
|
|
pathology of the heart due to hypothyroidism
|
myxedema heart due to interstitial mucopolysacharide.
|
|
|
what lab results indicate heart failure (not ischemia)
|
BNP elevated
creatinine and BUN elevated AST/ALT elevated |
|
|
clinical findings in R to L shunts
|
1- Cyanotic congenital heart disease
2- Inadequate oxygenation of blood cyanosis of skin and mucos membranes 3- Paradoxical emboli 4- Clubbing of fingers 5- Polycythemia= increased hct/RBC’s |
|
|
Causes of R to L shunts
|
1-Tetralogy of Falot= most common
2- Transposition of the great arteris (TGA) 3- Total anomalous pulmonary venous conection (TAPVC) 4- Tricuspid atresia 5- Persistant truncus arteriosis |
|
|
All left to right shunts have a ??
|
D in the name
|
|
|
all right to left shunts have a ???
|
T in the name
|
|
|
clinical findings of a left to right shunt
|
1- Cyanosis initially abscent
2- Increased pulmonary blood flow 3- Pulmonary HTN 4- Eisenmengers Syndrome= late cyanotic congenital heart disease. L to R shunt becomes a R to L shunt due to pulmonary HTN. |
|
|
causes of a left to right shunt
|
1- Ventricular septal defect= most common
2- Atrial septal defect 3- AV septal defect 4- Patent ductus arteriosus All of them have a D in the name |
|
|
complications of 22q11.2 deletions?
|
DeGeorge synd
Persistent truncus arteriosis |
|
|
what are the symptoms of Degeorge synd?
|
CATCH 22
-cleft palate -Absent Thymus -Cardiac anomalies -Hypoplasia of parathyroids (hypocalcemia) |
|
|
what gene is involved in 22q11.2
|
T-box
|
|
|
what gene is involved in williams disease
|
elastin gene
|
|
|
clinical manifestations of williams disease
|
-supravalvular stenosis
-facial abnormalities (elfin nose, puffy eyes, fat lower lip, round face, strabismus) |
|
|
most common ASD?
|
secundum type (90%)
|
|
|
what is the frequency and most common location for a VSD
|
20- 30%
membranous |
|
|
outcomes of VSD
|
Large:
-RV hypertrophy -Pulm HTN Small: -murmer -higher risk for endocarditis |
|
|
how do you chemically maintain a PDA?
|
Prostaglandin E
|
|
|
how do you chemically close a PDA
|
indomethacin or ibuprophen
|
|
|
presentation of PDA
|
machine like murmur
|
|
|
most common "cause" of AVSD
|
1/3 of downs syndrome children have it
|
|
|
what heart defect presents with a boot shaped heart?
|
Tet of Fallot
|
|
|
what gene is implicated in Tetrology of fallot?
|
notch genes
|
|
|
what type of transposition of the great arteries is stable?
|
if accompanied by VSD
|
|
|
tricuspid atresia
|
R to L shunt
complete occlusion of Tricuspid hypoplasia of RV high mortality |
|
|
clinical features of coarctation of the aorta
|
1- upper body hypertension
2- Hypotension of the legs -cold cyanotic legs, claudication, intermittant pain and limping brought on by walking. 3- Rib notching 4- murmur throughout systole with a thrill. 5- cardio megally due to LV hypertrophy. 6- berry aneurysm(circle of willis) 7- valvular defects |
|
|
what genetic defect predisposes you to coarctation of the aorta
|
turners syndrome (XO)
|
|
|
what is the "adult" form of coarctation of the aorta?
|
postductal
|
