exam 2 Flashcards
Hematocrit
volume of packed RBC expressed as a % of total peripheral blood
hemoglobin chains: types
Alpha, beta, gamma, epsilon
hemoglobin chains: factors
iron, vitamin b12, vitamin b6, folic acid
hemoglobin: cellular structure
porphyrin heme ring produced y mitochondria, iron inserted to form heme, globin chains produced by ribosomes and are joined to heme = hemoglobin
hemoglobin: levels
anemia = <13.5 g/dL for men, <12.5 g/dL for women. transfusion needed < 8 g/dL
anemia
reduction of hemoglobin in blood to below normal levels
anemia: pathogenesis (actions)
iron deficient, breast feeding, vegetarian diet, peptic ulcer, menorrhagia, pregnancy, carcinoma, gastrectomy
anemia: morphology
two ways
due to chronic disease: chronic inflammation and malignant condition
microcytic homochromic: decrease production of hemoglobin (iron, Hb, porphyrin ring)
types of anemia: aplastic
3 types
physiological changes
symptoms
what do they crave
idiopathic, secondary, primary (leukemia)
bone marrow depleted of hematopoietic cells and consists only of fibroblasts, fat cells, and scattered lymphocytes
uncontrollable infections, bleeding tendency, chronic fatigue, sleepiness, weakness
crave chewing ice cubes
types of anemia: macrocytic (megaloblastic)
low vitamin B12 or folic acid
folic acid: inadequate intake (green veggies and fruits), absorbed in jejunum, malabsorption caused by disease (alcoholics and elderly) and or increased demand (pregnancy, cancer)
b12: pernicious anemia: autoimmune due to autoantibodies against parietal cells and intrinsic factor, lack of gastric IF = stomach cancer or gastric bypass surgery, dx: Schilling test: oral radioactive b12 and cold b12; fatigue, short of breath, weakness, neurologic symptoms (can be fixed by therapy)
sickle cell anemia
substitution of glutamic acid by valine (point mutation), african americans (7-10%HbAS, 0.4% HbSS)
SHORT ANSWER: pathogenesis of sickle cell anemia
at low O2 partial pressures (venous side of circulatory system), abnormal HbS molecules crystallize into long, insoluble, polymerized rods, distorting shape of RBC, resulting in occlusion of capillaries, compromising O2 delivery to tissues which causes headaches, pain, cardiopulmonary insufficiency, recurrent infections, delayed intellectual development, neurologic deficits in children
thalassemia
genetic defect in the synthesis of HbA (adult hemoglobin) that reduces the rate of globin chain synthesis
alpha thalassemia: reduced synthesis of alpha chain of globin (gene deletion, usually 4 on chromosome 16)
one deletion: asymptomatic
two deletions: mild anemia with inc. RBC count
three deletions: severe anemia
four deletions: lethal in utero, hydrops fetalis
beta thalassemia: reduced synthesis of beta chain of globin
minor: hetero, mild and nonspecific symptoms
major: homo, severe and serious, chronic transfusions necessary
crew cut look
polycythemia
primary (polycythemia vera): clonal proliferation of hematopoietic stem cells, uncontrolled production of RBC (mutation; erythropoietin dec., always linked with blood cancer); symptoms due to blood hyperviscosity: blurry vision, headache, inc. risk of venous thrombosis, flush face due to congestion (plethora) and itching (eg. after bathing, inc. histamine
secondary: inc. RBC volume owing to bone marrow hyperplasia by inc. erythropoietin, caused by prolonged hypoxia; high altitudes, anoxia secondary to chronic lung disease (COPD), congenital heart disease
leukemia
WBC precursors in bone marrow and peripheral blood
types of leukemia: acute lymphoblastic
most common form in children, massive infiltration of bone marrow and peripheral blood with immature lymphoid cells (blasts)
good prognosis with chemo
types of leukemia: acute myelogenous
who does it affect
what physiological changes
prognosis
acid type
most common acute form in adults, clonal proliferation of myeloblasts in bone marrow (20%), fatal in 6 months with no treatment, all trans retinotic vitamin A acid
types of leukemia: chronic myelogenous
pluripotent hematopoietic stem cells, too many in peripheral blood and bone marrow, Philadelphia chromosome, tyrosine kinase inhibitors, transplant, chemo
types of leukemia: hairy cell
cells affected and how
+ for
sign
treatment
neoplastic proliferation of mature B cells, + for tartrate-resistant acid phosphate (TRAP); splenomegaly; good response to 2-CDA (chemo, adenosine deaminase inhibitor)
types of leukemia: chronic lymphocytic
lymphoid cells; lymph node involvement leads to generalized lymphadenopathy and is called small lymphocytic lymphoma; 7-9 years after dx
lymphoma
ages
organs affected
malignant or benign?
any age, lymph nodes, spleen, thymus, bone marrow, no benign types
types of lymphoma: non-Hodgkins: follicular
most common form, older people, slow growing, 7-9 years after dx
types of lymphoma: non-Hodgkins: diffuse-large cell
most common aggressive form; tissues infiltrated with large lymphoid cells that have irregular nuclear outlines and prominent nuclei
chemo
types of lymphoma: non-Hodgkins: Burkitt’s
malignant tumor of small B cells (EBV); extranodal masses, sub-saharan (jaw), abdominal mass; high mitotic index
“starry sky”
types of lymphoma: Hodgkins
ages
types (4)
special cells
prognosis
peaks at 25 & 55
4 types: nodular sclerosis, lymphocyte-rich, mixed cellularity, lymphocyte-depleted
Reed-Steinberg cells: bi or multilobed with a clear halo
Stage I & II have a good prognosis with chemo (90%)
lymphoma dx: PET grading
Stage I: involvement of single lymph node or group of nodes
Stage II: 2+ sites on same side of diaphragm
Stage III: both sides of diaphragm
Stage IV: widespread extralymphatic involvement (liner, bone marrow, skin, lung)
multiple myeloma
what is it
symptoms
tests
prognosis
malignant dx of plasma cells, 45+ years old
in bone marrow, destroys bones; punched out holes in skull, ribs, vertebrae
hypercalcemia, renal failure, proteinuria, infection, roleaux formation of RBC
xray (lytic lesions), urine with Bence Jones Protein (IgG), bone marrow biopsy (inc. plasma cells, fried egg)
fatal in 3-4 years by kidney failure or infection
ninlaro is a reversible proteasome inhibitor
bruised around eyes
hemophilia
sex-linked congenital clotting factor deficiency; uncontrollable bleeding with trauma and subcutaneous hematoma
A: deficiency of FACTOR VIII
B: deficiency of FACTOR IX
ECG: set up - leads
V1-6 and RA LA LL RL
ECG: conduction pathway
SA node sends out AP to AV node then to AV bundle (bundle of HIS) then R&L branches then Purkinje fibers
ECG: know graph, and what each section does
P wave: depolarization of atria
PR interval: depolarization of atria and delay at AV junction
QRS complex: depolarization of ventricles
ST segment: period between ventricular depolarization and beginning of repolarization
T wave: repolarization of ventricles
R-R interval: time between two ventricular depolarizations
ECG: chronotropic
heart rate (- = beta blocker)
ECG: inotropic
cardiac contractile force
ECG: dromotropic
speed of impulse transmission
Atrial septal defect
cause
blood direction
failure of proper closure of foramen ovale or defect in the septum
blood from LA to RA due to pressure difference
Ventricular septal defect
failure of fusion of interventricular septum
high pressure, blood shunts
Tetralogy of Fallot
stenosis of RV outflow tract, RV hypertrophy, VSD, overriding aorta
R to L shunt: cyanosis
squat during spells (inc. arterial resistance)
Valvular disease: rheumatic fever
cause
pathogenesis
dx
systemic complication of pharyngitis due to group A (beta-hemolytic) streptococci, 2-3 weeks after strep
molecular mimicry of bacterial M protein, acts like proteins in human tissue
dx with Jones’ criteria, 1-2 major, 1 minor
major: carditis, previous group A strep, polyarthritis, erythema
minor: fever, ECG changes
bacterial endocarditis
inflammation of endocardium due to bacterial infections (strep. viridans)
bacterial endocarditis: subacute infective
low virulence organisms, do not destroy valves, mild symptoms (low fever)
bacterial endocarditis: acute infective
highly virulent organism, infect normal valves (most commonly tricuspid), destroy valves (strep. aureus)
fever with chills, murmurs, need antibiotics
bacterial endocarditis: by staph. epidermidis
endocarditis of prosthetic valves
pericarditis
causes
symptoms
ecg changes
viruses, travel, bacteria, open heart surgery
chest pain worse with lying supine and with inspiration
concave ST elevation with PR depression, normal CK-MB
myocarditis
what causes it
what is it
physiological changes
treatment
viruses, parasites, and protozoa
inflamed heart muscle, abrupt onset, may lead to acute heart failure
myocardial degeneration and necrosis with mononuclear inflammatory infiltrate
treat underlining cause
dilated cardiomyopathy
what is it
causes
dilation of all 4 chambers and most common form, systolic dysfunction
causes: idiopathic, genetic mutation, myocarditis, pregnancy, alcohol abuse
hypertrophic cardiomyopathy
LV hypertrophy due to genetic mutation in sarcomere proteins (contract/relax)
most common is autosomal dominant
diastolic failure due to decreased cardiac output
death in young athletes, syncope with exercise, ventricular arrhythmias
restrictive cardiomyopathy
what is it
causes
decreased compliance of ventricular endomyocardium that restricts filling during diastole
cause: amyloidosis, result in CHF with decreased QRS amplitude
nonrheumatic aortic stenosis
cause
area of heart
physiological change
results in…
cause: congenital bicuspid aortic valve abnormality, calcified aortic stenosis
strain on LV = heart failure
aortic stenosis caused by degenerative changes in valve leaflet connective tissue and calcification
result in cor pulmonale
cor pulmonale
overload of RV from pulmonary hypertension
atherosclerosis
plaque build up in arteries
atherosclerosis pathogenesis
injury to blood vessel by reactive O2 species (ex: oxidized CDL, free radical, neutrophils/leukocytes/platelets) go to injury site and cause inflammation
macrophages consume oxidized CDL and become foam cells which release growth factors (cytokines) to stimulate movement of smooth muscle cells which proliferate and contribute to plaque
TPA produced endothelial cells dissolve plaque
complications: plaque rupture = thrombus formation
turbulent flow = aneurysm3
Coronary Artery Disease/CHD/Ischemic HD
what is it
who is at risk
levels
lipid deposits in large coronary arteries, accumulate by diffusion
obesity, type A personality, cocaine induced arrhythmias
LDL, HDL, and homocysteine inc., inc. risk of atherosclerosis
dec. blood supply to heart, prolonged= MI
SHORT ANSWER
manifestations of CAD: angina pectoris - stable angina
what is it
cause
symptoms
exertion, gone with rest, relieved by nitroglycerine
due to atherosclerosis of coronary artery with >50-60% stenosis, dec. blood flow
no necrosis of myocytes, <15 mins, arm/jaw pain, diaphoresis, short of breath, ST segment depression
SHORT ANSWER
manifestations of CAD: angina pectoris - unstable angina
more frequent, longer, less relieved by nitro, rupture of atherosclerotic plaque with thrombosis and incomplete occlusion of coronary artery
higher chance of MI
SHORT ANSWER
manifestations of CAD: angina pectoris - Prinzmetal’s
at rest by coronary artery spasm, relieved with nitro or calcium channel blockers
ST segment elevation during chest pain and gone when pain has subsided
SHORT ANSWER
manifestations of CAD: angina pectoris - TREATMENT
oxygen, baby aspirin, nitroglycerine, morphine
aneurysm
dilating of artery wall or outpouching portion of wall
arteriosclerotic aneurysm
weakens vessel wall (most acquired as a result of arteriosclerosis)
dissecting aneurysm of aorta
splitting of aorta media by blood due to degenerative changes that cause layers to lose cohesiveness and separate
abdominal aortic aneurysm
cause
symptoms
result of atherosclerosis
abdominal pain, back/flank pain, hypotension, urge to defecate (pressure on large intestine)
atheroma
degeneration of artery wall due to atherosclerosis
myocardial infarction
areas involved
percents
L&R ventricles: anterior, posterior, and lateral walls
regional (90%), diffuse (10%)
myocardial infarction: L anterior descending artery (LAD)
infarction of anterior wall and septum of LV
most commonly involved artery in MI
myocardial infarction: R coronary artery (RCA)
infarction of posterior wall and septum, and papillary muscles of RV
2nd most commonly involved artery
myocardial infarction: L circumflex artery
infarction of LV lateral wall
SHORT ANSWER
MI ECG zones (3)
zone of ischemia: ST segment depression with or without T wave inversion
zone of injury: ST segment elevation with or without loss of R wave
zone of infarction: deep Q waves due to absence of depolarizing current from dead tissue and receding currents from opposite side of heart
MI dx
enzyme tests, leak with proteins from necrotic cells when muscle becomes infarcted
Troponin T & I (protein)
creatine kinase CK-MB (enzyme)
lactic dehydrogenase (enzyme)
MI treatment
thrombolytic therapy to dissolve clot
coronary angioplasty (balloon pushes plaque into walls)
bypass surgery (bypass obstruction with segments of saphenous vein from leg)
anticoagulant
beta blockers (reduce myo irritability)
aspirin (inhibit platelet function)
antiarrhythmics (reduce myo irritability)
pacemaker (if complete block)