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IMS Exam 2 > IMS Exam 2 > Flashcards

IMS Exam 2 Flashcards

1
Q

Name the atrial waves

A

A-wave - atrial contraction
C-wave - bulging of AV valve into atria during systole
V-wave - filling of atria

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2
Q

What is systole?

A

Ventricular contraction

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3
Q

What is diastole?

A

Relaxation

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4
Q

What is isovolumetric contraction?

A

All the valves are closed

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5
Q

What is isovolumetric relaxation?

A

Period where semilunar valves close & AV valves open

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6
Q

Define EDV (End Diastolic Volume)

A

Volume of blood in ventricle before contracting

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7
Q

Define ESV (End Systolic Volume)

A

Amount of blood that remains in ventricle after contraction

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8
Q

What is central venous pressure?

A

aka R atrial pressue

inc. in CVP = dec. in CO

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9
Q

What is HR controlled by?

A
  1. Baroreceptors (in aortic arch, carotids)
  2. Atrial & ventricular sensors that respond to V changes
  3. CNS activation (stress, fear, excitement)
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10
Q

Define preload

A

Amount of blood returned to the heart

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11
Q

What is contractility dependent on?

A
  1. Amount of contractile proteins
  2. ATP
  3. Ca
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12
Q

Risk factors for CAD

A

i. Age M > 45, W > 55
ii. Family History
iii. High Cholesterol
iv. Smoking
v. High Blood pressure
vi. Diabetes
vii. Obesity
viii. CAD risk equivalents

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13
Q

What is angina?

A

ischemia that doesn’t kill cells

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14
Q

Characteristics of mitral stenosis

Cause?

A 
cause = rheumatic fever
effects:
1. L atrial enlargement
2. Pulmonary HTN
3. R heart failure

low pitch diastolic rumble at apex

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15
Q

Characteristics of mitral regurgitation

A

causes: rheumatic fever, infective endocarditis, mitral valve prolapse, acute MI, LV dysfunction

effects:

  1. L atrial enlargement
  2. Pulmonary HTN
  3. R heart failure

high pitched pansystolic blowing murmur

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16
Q

Characteristics of aortic stenosis

A

cause: senile calcification
effects: LV dysfunction

crescendo-decrescendo systolic murmur

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17
Q

Characteristics of aortic regurgitation

A

causes: same as mitral regurgitation
effects: LV dysfunction

high pitch blowing murmur heard during systole

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18
Q

Characteristics of tricuspid regurgitation

Cause

A

causes: endocarditis (IV drug use), inc. pulmonary pressures
effects: R heart failure

systolic mumur

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19
Q

How to treat valvular disease?

A
  1. Valve replacement
  2. Valve repair
  3. TAVR - Transcatheter aortic valve replacement
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20
Q

Characteristics of Hypertrophic cardiomyopathy

A

Most common genetic CV disease; thickened LV

effects:

  1. CHF
  2. Syncope
  3. SCD

Treat w/ Defibrillator

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21
Q

Characteristics of Dilated cardiomyopathy

A

Most common; idiopathic
Systolic dysfunction

Enlargement of 1 or both ventricles

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22
Q

Characteristics of restrictive cardiomyopathy

A

Amyloidosis, Sarcoidosis
Diastolic dysfunction

Inc. stiffness of ventricular walls

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23
Q

Characteristics of arrythmogenic R ventricular dysplasia

A

genetic

fibrofatty infiltration of RV

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24
Q

Characteristics of cardiac tamponade

A

compression of heart from accumulation of cardiac fluid

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25
Q

Pericarditis

A

inflammation from virus/idiopathic

ST elevation on every lead w/ PR depression

treat w/ NSAIDS

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26
Q

Causes of heart failure

A
  1. CAD
  2. HTN
  3. Idiopathic
  4. Valvular
  5. Respiratory (R Heart failure)
  6. Anemia
  7. Endocrine
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27
Q

Compensatory mechanisms of Heart failure

A
  1. SNS activation
  2. Inc. preload
  3. Hypertrophy
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28
Q

L Heart failure

A 
Causes:
1. CAD
2. HTN
3. Valvular disease
Symptoms
1. Dyspnea/DOE
2. Paroxysmal Nocturnal Dyspnea
3. Orthopnea 
4. Pleural effusion
5. Crackles
6. Edema

inc. in ESV/dec in LV cavity = inc L atrial pressure

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29
Q

R Heart Failure

A 
Causes
1. L heart failure/pulmonary disease
2. COPD
3. Obstructive sleep apnea
4. pulmonary HTN
5. Pulmonay fibrosis
Symptoms
1. Edema
2. Dyspnea
3. JVD (jugular venous distension) 
4. Ascites
5. Hepatomegaly/splenomegaly
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30
Q

Biventricular failure

A

L heart failure causing R heart failure

Cor Pulmonale & L HF

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31
Q

How to treat CHF?

A 
Meds
1. ACE inhibitors/angiotensin receptor blockers
2. Beta blockers
3. Loop diuretics
4. Aldosterone antagonists
Devices
1. Defibrillator
2. Pacemaker
3. Left Ventricular Assist Device (LVAD)
Heart transplant
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32
Q

Sinus Tachycardia

A

Causes

  1. Fever
  2. Pain
  3. Hyperthyroidism
  4. HOTN

> 100 bpm

Treat underlying cause

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33
Q

Sinus Brachycardia

A

Causes

  1. Athletes
  2. Sleep meds
  3. Electrolytes

<60 bpm

Not treatable

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34
Q

Sinus Arrhythmia/Arrest

A

Sinus Arrhythmia/Arrest
1. Respiratory

fast or slow..bipolar
>4 sec pause = arrest

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35
Q

Systolic dysfunction

A
  1. MI
  2. Dec. ATP

dec./impaired contractility

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36
Q

Diastolic dysfunction

A
  1. Ca influx during relaxation
  2. LV filling from
    a. fibrosis
    b. hypertrophy
    c. scarring of LV

impaired relaxation

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37
Q

Mechanisms of arrythmias

A
  1. Automaticity
  2. Triggered activity
    Early afterdepolarizations - AP before cell is repolarized
    Late afterdepolarizations - AP before AP would normally occur
  3. Reentry - impulse doesn’t leave & causes another AP…most common form of arrythmias
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38
Q

What are escape rhythms?

A

SA nodes fail & other pacemaker cells take over

  1. Junctional (40-60 bpm)
  2. Ventricular (20-40 bpm)
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39
Q

Atrial Fibrillation

A

Risk for thromboembolism
stagnant blood

Irregular HB & irregular rhythm
loss of atrial kick - dec. CO

anticoagulants

no P waves

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40
Q

Atrial Flutter

A

Regular HB & irregular rhythm
Atrial rate 240-350 bpm
variable vent. Rate 150 bpm
sawtooth pattern

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41
Q

Ventricular tachycardia

A

Causes

  1. MI
  2. Ischemia

3 or more PVCs
turns into Vfib if untreated

irregular HB, regular rhythm
rate = 120-250 bpm = deadly

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42
Q

Ventricular fibrillation

A

irregular HB, irregular rhythm
Results in death
Torsades do points -R meets T

Magnesium

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43
Q

AV block

A

Disturbance btwn sinus impulse & ventricular response

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44
Q

1st degree AV block

A

Prolonged PR interval >0.2 sec

Not pathologic, not treatable

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45
Q

2nd degree AV block

A

some atrial impulses are not conducted to the ventricles

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46
Q

Type I 2nd degree AV block

A

-usually due to reversible ischmia of the AV node

progressively prolonged PR interval w/ dropped beat

rarely requires treatment

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47
Q

Type II 2nd degree AV block

A

Consistent PR interval w/ dropped beats & non conducted P waves

needs treatment - often progresses to 3rd block

Usually assoc. w/ pathologic lesion in bundle of His, R bundle branch or both

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48
Q

3rd degree AV block

A

P waves don’t correlate w/ QRS complex

no impulses conducted from atria to ventricles

requires pacemaker

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49
Q

Accessory Pathways

A

something that conducts beats into the ventricles other than the AV node

no filtering & slowing from the AV node

ex. WPW

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50
Q

Wolff-Parkinson White syndrome

A

accessory pathway that bypass the AV node

Delta waves - up slurring of initial R wave

can cause supraventricular tachycardia

treat w/ ablation

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51
Q

Treatment of arrhythmias

A 
Antiarrhythmic meds
1. Na channel blockers
2. beta blockers
3. Ca channel blockers
4. K channel blockers
5. Amiodarone most widely used
Invasive procedures
6. Cardioversions - shock back to normal
7. Ablation
8. Pacemakers
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52
Q

Define shock

A

Life-threatening condition…insufficient delivery of ox. blood to the body = tissue hypoxia & cellular dysfunction

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53
Q

Cardiogenic shock

A

Causes:

  1. MI
  2. End-stage cardiomyopathy/HF
  3. Ventricular rupture
  4. Congenital defects

low CO w/ high LV preload leading to pulmonary edema, HOTN

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54
Q

Obstructive Shock

A

Causes:

  1. PE - acute R HF
  2. Cardiac tamponade
  3. Tension pneumothorax

mechanical obstruction of heart (usually R)

anticoag, thrombolytics, pericardial window, chest tube

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55
Q

Hypovolemic Shock

A

Causes

  1. Internal loss/hemorrhage
  2. Fracture of large bones
  3. 3rd spacing - leaking of fluid into interstitial space
  4. External hemorrhage
  5. Burns
  6. Severe vomiting, diarrhea, diuresis

dec. in blood V enough to cause hypoxia

  1. Crystalloid fluid (electrolytes)
  2. Blood: Packed RBCs
  3. Stop source of fluid loss, replace blood V
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56
Q

Types of distributive shock

A

Extreme vasodilation/HOTN

  1. Anaphylactic
  2. Neurogenic
  3. Septic
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57
Q

Anaphylactic shock

A 
Causes
1. Drugs
2. Tree nuts, insect bites, animals 
1/3 no clear cause
rxn w/in 2-30 min of Ag exposure 
Effects
1. HOTN
2. Bronchospasms
3. Tachycardia/tachypnea
Ag/IgE rxn; vasodilation
vasodilation - vasculature permeable
fluid lead into interstitial space
Treatment
1. Mgmt of airway
2. Epi pen
3. Antiinflammatories (Steroids)
4. Antihistamines
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58
Q

Neurogenic Shock

A 
Cause
1. Brain trauma
2. Spinal cord injury
3. Drug overdose
Effect
1. Vasodilation
2. HOTN
3. Intrinsic control of BP & HR

Orthostatic HOTN - BP drops upon standing, HR inc
Loss of sympathetic tone on peripheral vasculature

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59
Q

Septic Shock

A

Gram - worst
Gram +/fungal

Portals:

  1. GU & GI
  2. Respiratory tract
  3. Skin

SIRS + Bacteremia + Hemodynamic instability/organ dysfunction

Treatment

  1. Fluids
  2. Vaso-pressores
  3. Broad-spectrum antibiotics
  4. Glucocorticoids (steroids)
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60
Q

SIRS criteria

A

Systematic Inflammatory Response Syndrome
2 or more:
1. Temp 38
2. HR >90 bpm
3. Resp rate >20/min or PCO2 12000 or 10% bands

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61
Q

Where are platelets stored?

A

In the spleen, about 1/3 or storage

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62
Q

What stimulates erythrocyte production?

A

Erythropoietin….secreted by kidney

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63
Q

What is the sequence of hematopoiesis?

A

Proerythroblast to basophil erythroblast to polychomotophil to reticulocyte..in peripheral tissue = erythrocyte

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64
Q

How are RBCs produced in the fetus?

A

1st trimester - yolk sac
2nd trimester - liver & spleen
3rd trimester - red marrow

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65
Q

How much oxygen is 1 g of hemoglobin?

A

1.34 mL O2/g Hgb

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66
Q

What nutrients are required for erythropoiesis?

A 
Folate
B12
iron
protein
vitamins 
minerals
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67
Q

What stimulates kidney to secrete EPO?

A
  1. low levels O2
  2. inc. in exercise
  3. Loss of lung tissue in emphysema
  4. drop in RBC count
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68
Q

How are RBCs broken down?

A

In spleen

  1. Methemoglobin is removed by leukocytes
  2. Globin is broken down into amino acids & iron recycled
  3. Porphyrin is reduced to bilirubin
    - conjugated bilirubin is excreted in bile
    - conj. bili converted to urobilinogen by intestinal bacteria && excreted in stool/urine
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69
Q

What is hemoglobin composed of?

A
  1. 2 pairs of polypeptide chains
  2. globins w/ heme molecule
  3. iron
  4. protoporphyrin
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70
Q

Oxy Hbg curve shift to left

A

what you see in lungs

  1. Low pCO2
  2. High pH, low [H+]
  3. Low 2,3 BPG
  4. Low temp
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71
Q

Oxy Hgb curve shift to right

A

what you see in muscles - when body needs O2

  1. High temp
  2. High 2,3 - BPG
  3. High CO2
  4. Low pH, high [H+]
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72
Q

How is CO2 found in the body?

A
  1. Dissolved gas
  2. Bicarbonate ion
  3. Bound to hemoglobin
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73
Q

Relative vs. absolute anemia

A

R - normal total RBC mass w/ disturbances in regulation of blood volume

A - actual dec. in #s of RBC

  1. dec. production or
  2. inc. destruction
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74
Q

Aplastic anemia

A

Stem cell disorder
low RBC, WBC & platelets
Toxic, radiant or immonologic injury to bone marrow stem cells

Diagnose w/ bone marrow Bx
Fatal unless bone marrow transplant

  1. ID & avoid toxic exposure
  2. HLA & ABO for donors
  3. Immunosupressive therapy
  4. Stimulate hematopoiesis
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75
Q

Anemia of chronic renal failure

A

no EPO!
dec. RBC count w/ low Hct & Hgb

Treat w/

  1. Dialysis
  2. EPO
  3. Replacement of iron, folate, B12
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76
Q

Anemia related to Vit B12/folate deficiency

A

disruption of DNA synthsis produces megaloblasts..macrocytic
Pernicious anemia due to lack of intrinsic
factor leading to B12 deficiency

Folate def from alcoholism, cirrhosis, pregnancy, infancy
folate def assoc. w/ neural tube defects

Treat underlying cause…give supplements!

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77
Q

Iron deficiency anemia

A

Most common nutritional deficiency
No Hgb synthesis
Hypochromic, microcytic RBCs
low MCV, MCH, MCHC

pica - crave weird food
Koilonychias - spoon shaped nails
blue sclerae

Give iron

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78
Q

Thalassemia

A

Inc. RBC destruction
mutant genes suppress globin synthsis

hypochromic, microcytic RBCs
low MCV, MCH, MCHC

  1. Blood transfusions
  2. Splenectomy
  3. Chelation therapy
  4. Bone marrow transplant
  5. Genetic counseling
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79
Q

Sickle Cell Anemia

A

Genetics
Sickle cell - vascular occlusion

  1. Stem cell transplant
    Death if no transplant
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80
Q

Hereditary Spherocytosis

A

Defective RBC membrane, altered cell metabolism

Autosomal dominant
[Hgb] inc.

  1. Splenectomy
    Cured but watch for infection
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81
Q

G6P Dehydrogenase deficiency

A

Genetic
RBC membrane destruction
most common

Preventative

  1. Avoidance of drugs that trigger hemolysis
  2. Aggressive infection mgmt
    * fava bean susceptibility
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82
Q

Primary Polycythemia Vera

A

Neoplastic transformation of bone marrow stem cels
inc in RBCs, WBCs, thrombocytosis
inc uric acid

inc. viscocity

Treatment

  1. Reduce increases in blood volume
  2. Phlebotomy
  3. Radioactive phosphorus
  4. Chemotherapeutic agents
83
Q

Secondary Polycythemia Vera

A

chronic hypoxemia = inc. EPO
inc. RBC count

Treatment

  1. ID why hypoxic
  2. Phlebotomy if necessary
84
Q

Relative Polycythemia Vera

A

Dehydration w/ fake inc. in RBCs
elevated Hct, Hgb

  1. Treat underlying cause
  2. Fluid administration
85
Q

Stages of hemostasis

A
  1. Injured vessel constricts, formation of platelet plug
  2. Fibrin clot forms from intrinsic & extrinsic pathways - coagulation
  3. Clot retraction
86
Q

Define hemarthrosis

A

Bleeding into a joint

87
Q

Define telangiectasia

A

lesion created by dilation of capillaries & small arteries

-weakened collagen

88
Q

Define petechiae

A

flat, nonblanching red or purple spots caused by capillary hemorrhages in the skin & mucous membranes

89
Q

Define Purpura

A

groups of petechiae

often itchy

90
Q

Define ecchymosis

A

bruise - blood escapes into the tissues

91
Q

What is the effect of aspirin on hemostasis?

A

inhibits platelet function

would extend bleeding time

92
Q

Define hematoma

A

a raised bruise

93
Q

What is Ehlers-Danlos syndrome?

A

deficient collagen & elastin

skin bruises easily & damaged blood vessels

94
Q

Relate Vitamin C to vascular pupura

A

Vitamin C deficiency causes defective collagen synthesis, inc. vascular permeability = petechiae & bleeding

95
Q

What is hereditary hemorrhagic telangiectasia

A

autosomal dominant
dilated small blood vessel that easily bleeds
vessel walls w/ single layer of endothelium - deficient support

96
Q

Mechanisms of thrombocytopenia

A
  1. Immune
  2. Dec. platelet production
  3. Dec. platelet survival
  4. Splenic sequestration
  5. Dilution of circulating platelets
97
Q

Causes of thrombocytopenia

A
  1. Bone marrow suppression from chemo
  2. Recent immunizations
  3. Alcohol
  4. B12 & folate deficiency
98
Q

Effects of thrombocytopenia

A
  1. Low platelet count
  2. Prolonged bleeding time
  3. Petechiae
  4. Purpura
99
Q

Types of thrombocytosis

A
  1. Transitory - stress/physical exercise
  2. Primary - polycythemia vera/leukemia
  3. Secondary - response to hemorrhage, disease process or hemorrhage
100
Q

Risks of thrombocytosis

A
  1. Thrombosis

2. Pulmonary Embolism

101
Q

What are the coagulation disorders?

A
  1. problems w/ formation, stabilization or lysis of fibrin clot
  2. inappropriate activation of coagulation cascade (excessive clot formation)
102
Q

Hemophilia

A

A - factor VIII deficiency, X linked recessive
-treat w/ cryoprecipitate or factor VIII precipitate

B - Factor IX deficiency, FFP or cryoprecipitate

-hemarthrosis, inc. PTT

103
Q

Von Willebrand disease

A

autosomal dominant of Factor VIII & platelet dysfunction

causes excessive bleeding

prolonged bleeding time, prolonged PTT

104
Q

Vit K Deficiency Bleeding in Infancy

A

Effects

  1. Melena
  2. Umbilical bleeding
  3. Hematuria
  4. Intracranial hemorrhage
  5. Hypovolemic shock

Treatment

  1. Vit K
  2. FFP or whole blood
105
Q

Vitamin K Deficiency

A 
Fat soluble vitamin
Causes
1. malnutrition/malabsorption
2. hepatic disease
3. antibiotic therapy
4. oral anticoagulation therapy

Excessive bleeding
PT/INR inc. but other studies normal

Treatment

  1. Vit K
  2. Treat underlying condition
106
Q

DIC

A 
Disseminated Intravascular Coagulation
Clotting & bleeding occurs at the same time
Causes
1. Trauma
2. Malignancy
3. Burns
4. Shock

widespread clots in small vessels so factors & platelets used up

inc. bleeding time
inc. PT/INR, PTT, D-dimer

Treatment

  1. Removal/correct underlying cause
  2. Support major organs
  3. FFP, packed RBCs, platelets, cryoprecipitate
107
Q

Hepatic disease & hemostasis

A

Coagulopathies result from:

  1. impaired abs. of vit K
  2. dec. synthesis of fibrinogen, factors V & XI
  3. inability to remove activated factors

Treatment

  1. Vit K
  2. Platelet transfusion, FFP, whole/packed blood
108
Q

Describe the layers of blood vessels

A

Tunica:

  1. Intima - endothelial in direct contact w/ blood
  2. Media - smooth muscle (thickest in arteries)
  3. Adventitia - collagen (thickest in veins)
109
Q

What is the equation for blood flow

A 
Flow = Velocity x A 
A=cross sectional area
-diseases reduce A
inc. w/ vasodilation
dec. w/ vasoconstriction
110
Q

Bruit vs. thrill

A

B - can hear turbulence of blood

T - can feel turbulence of blood

-could be caused by plaque buildup/clot

111
Q

What is the critical closing pressure?

A

blood flow stops

20 mm Hg

112
Q

What is blood vessel compliance?

A

the ability to accept an inc. of blood volume

113
Q

Define edema

A

an inc. in capillary fluid pressure (hydrostatic pressure)

114
Q

Define lymphadema

A

inc. in fluid in intersitium caused by impairment of lymphatic flow

115
Q

Cardiac output

A

The amount of blood leaving the heart

=SV x HR

116
Q

What is preload?

A

amount of blood returned to the heart

End-diastolic volume

117
Q

What is afterload?

A 
systemic vascular resistance
dependent on:
1. radius of arteries
2. degree of vessel compliance 
major determinant of diastolic pressure
118
Q

what is mean arterial pressure?

A

MAP
calc. ave. pressure w/in the circulatory system
(2 x diastolic P) + systolic P

119
Q

Auscultation of Korotkoff sounds

A

Systolic P: onset of Korotkoff sounds

Diastolic P: disappearance of sounds

120
Q

Short-term regulation of BP

A
  1. SNS - release of E & NE, bind to alpha receptors for vasoconstriction & inc. SVR
  2. PSNS slows heart
  3. Vasomotor center - baroreceptors
    betareceptors for inc. HR
121
Q

How is long-term BP regulated?

A
  1. neural, hormonal, renal
  2. inc. in ECF = inc. CO & SVR = inc. BP
    kidneys excrete excess Na & fluid
  3. Renin-angiotensin aldosterone system - low P causes hormones, inc. Na & water resorption, inc in SVR
122
Q

Causes of orthostatic HOTN

A
  1. Problem w/ vasomotor/baroreceptor response
  2. Adverse effect of drug therapy
  3. Arterial stiffness
  4. Dec. in V
  5. Secondary disease process
  6. Vasovagal rxn
  7. Cardiac dyshythmias
123
Q

BP classification

A

Normal 160 >100

124
Q

Define hypovolemic

A

state of dec. blood volume

125
Q

Changes in systolic/diastolic P

A

S - V issues

D- Vascular resistance issues

126
Q

Secondary HTN

A

HTN due to different disease state

usually a renal issue

127
Q

Arterial vs. venous thrombosis

A

A - ischemia

V - edema

128
Q

Thrombus vs. embolus

A

T - stationary clot

E - traveling clot

129
Q

Define vasospasm

A

sudden constriction of arterial smooth muscles resulting in obstruction of flow

130
Q

Formation of plaque

A
  1. Injury to artery
  2. Monocyte adherence
  3. Disruption of endothelium
  4. Activation of Growth Factor
  5. Smooth muscle proliferation
  6. Accumulation of lipids
  7. Origination of mature plaque
  8. Intrusion into the lumen
131
Q

Thromboangitis Obliterans (Buerger Disease)

A

rare inflammatory condition of blood vessels
results in varying degrees of obstruction

Treatment

  1. Smoking cessation
  2. Prostaglandins
132
Q

Raynaud Syndrome

A

extreme vasoconstriction of digits

133
Q

True vs. false aneurysm

A

T - affect all 3 tunica

F - does not affect all 3 tunica, due to trauma

134
Q

Define dissection

A

Blood vessel layers separate & flow goes through, can rupture

135
Q

Acute arterial occlusion

A

Absence of arterial circulation = emergency

may result from thrombi/emboli or mechanical compression

136
Q

HIV-1 vs HIV-2

A

1 - more common in Western world
most virulent - at least 10 subtypes

2 - common in W Africa
longer latency/asymptomatic period
-milder & lower mortality rates

137
Q

CCR5 delta 32

A

if you have both alleles

immune to HIV

138
Q

CCL3L1

A

if deficient, more susceptible to HIV

139
Q

PEP of HIV

A

post exposure prophylaxis

  1. Atripla
  2. Admin of 2-3 meds for 4 wks/longer
140
Q

Describe HIV structure

A

Core - nucleocapsid
2 RNA strands = retrovirus
-reverse transcriptase w/ polymerase & ribonuclease
protease clips p55 to make it infectious & activate virions
contains at least 9 genes
lipid bilayer viral envelope

141
Q

envelope of HIV

A

membrane drived from host cell

contains proteins gp120 & gp41 that looks like self

142
Q

HIV mechanism

A
  1. gp 120 bings to CD4 receptors & refolds
  2. combines w/ CCR5 or CXCR4 to fuse w/ cell by chemokine receptors
  3. gp41 implants it into cell membrane
  4. virus core injects it into cytoplasm
  5. RNA to DNA
  6. Integrase splices DNA & puts it into host’s genome
143
Q

Why can’t antibodies bind to HIV?

A

gp120 & gp41 are bound together

144
Q

Symptoms of primary HIV infection

A
  1. Flu/mono like symptoms
  2. Rash
  3. Pharyngitis

CD4 count >400cells/uL
Dec. # of WBCs
inc. in CD8 T cells

145
Q

AIDS prognosis

A
  1. CD4 count <200
  2. 1 or more opportunistic infections
  3. 1 or more tumors/cancers
146
Q

CDC HIV classification system

A

CD4 T-cell count
Cat. 1: >500
2: 200-499
3: <200

clinical categories
A: not so bad infections
B: secondary infections
C: conditions listed in AIDS surveillance case definition

147
Q

Child Clinical HIV categories

A

N: asymptomatic
A: mildly asymptomatic w/ 2 or more symptoms
B: moderately symptomatic w/ some opportunistic infections
C: severely symptomatic w/ AIDS

148
Q

Diagnostic testing for AIDS

A
  1. ELISA
  2. Western - confirms ELISA
  3. OraQuick - must be conf. by Western
149
Q

Name a common cause of diarrhea in HIV Pts

A

protozoa cryptosporidium

150
Q

What is the most common opportunistic infection in HIV Pts?

A

opportunistic pneumonias

151
Q

What is normally the 1st symptom of HIV infection?

A

Exanthem - rash

152
Q

What are the classes of drugs used to treat AIDS?

A
  1. Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
  2. Nonnucleoside Reverse Transcriptase Inhibitors (NNRTIs)
  3. Protease Inhibitors (PIs)
  4. Fusion Inhibitors
  5. Integrase Strand Transfer Inhibitors (INSTIs)
  6. CCR5 antagonists
153
Q

Why is tropism testing needed for starting AIDS med. therapy?

A

ex. Maraviroc
-CCR5 antagonists
drug does not work on those w/ CXCR4-tropic HIV

154
Q

How does NRTIs work?

A

prevent replication by preventing HIV DNA synthesis

155
Q

How does NNRTIs work?

A

changes conformational shape of enzyme

affects CYP450 system & has CNS side effects

156
Q

How do PIs work?

A

Blocks cleavage of p55 to make it infectious
Check for HLA
interacts w/ CYP450

157
Q

How do fusion inhibitors work?

A

blocks virus from binding

158
Q

What is the optimal AIDS therapy?

A 
2 nucleosides & 1 of either:
Boosted PIs
NNRTI
INSTI
CCR5 antagonist
159
Q

What is the function of the nasal cavity?

A
  1. Conduct gases to & from lungs

2. Filter, warm & humidify air

160
Q

What is the function of the paranasal sinuses?

A

4 sinuses containing air

  1. Provide speech resonance
  2. Inc. heat & water vapor exchange surfaces

swept clean by cilia

161
Q

Nervous system control of lungs

A

ANS - controls bronchi & bronchiole muscles

parasympathetic - vagus nerve, constriction of muscle (ACh)

sympathetic - relaxation of smooth muscle (B2 adrenergic receptors)

162
Q

Define recruitment

A

opening of closed capillary vessels

163
Q

Define distension

A

widening of pulmonary capillary vessels

164
Q

Control of ventilation

A
  1. Respiratory centers in pons & medulla
  2. Pneumotaxic center
  3. Apneustic center
  4. Central chemoreceptors
  5. Peripheral chemoreceptors
  6. Hering-Breuer refelx
  7. Proprioceptors
  8. Baroreceptors
165
Q

Central vs. peripheral chemoreceptors

A

C - located in medulla, responds to changes in CO2 & pH

P - located in aortic arch & carotid bodies, respond to dec. in arterial O2

166
Q

Pneumotaxic vs. apneustic centers

A

both located in pons

P - influences rate of respiration

A - influences pattern of respiration

167
Q

What is the function of the Hering-Breuer reflex?

A

to prevent overdistension of the lungs

168
Q

Types of ventilation-perfusion imbalances

A
  1. High - alveoli are ventilated but not perfused
  2. Low - Underventilated, airways partially obstructed
  3. Shunt - no ventilation
169
Q

Barriers of alveolar-capillary membrane

A
  1. Surfactant
  2. Alveolar membrane
  3. Interstitial fluid
  4. Capillary membrane
  5. Plasma
  6. RBC membrane
170
Q

Define hypoxemia

A

low arterial O2 & low Hgb saturation

171
Q

Define hypoxia

A

dec. in tissue oxygenation

172
Q

Define ischemia

A

dec. in perfusion to tissue

173
Q

What is a saddle embolus?

A

occlusion of the main pulmonary artery

174
Q

Which lung cancers can be treated w/ surgery if caught early?

A

Squamous cell carcinoma & adenocarcinoma

175
Q

How long of symptoms for chronic bronchitis?

A

chronic/recurrent productive cough >3 mo for more than 2 years

176
Q

Who are blue bloaters?

A

Pts w/ chronic bronchitis

177
Q

What is extrinsic asthma caused by?

A

allergies

Type I sensitivity rxn

178
Q

Define emphysea

A

abnormal permanent enlargement of air spaces distal to the terminal bronchiole accompanied by destruction of their walls
-imbalance btwn proteases & antiproteases
alpha1-antitrypsin
smoking inhibits this enzyme
-no symptoms unless 1/3 of lung incapacitated

-loss of capillaries & surface area

179
Q

Who are pink puffers?

A

emphysema Pts

180
Q

Define bronchiectasis

A

chronic, necrotizing infection of the bronchi & bronchioles

  • abnormal dilation of airways - permanent
  • H influenza is most common infection
181
Q

Define bronchiolitis

A

inflammation of bronchioles from infectious agents

most common: RSV

182
Q

Define Cystic Fibrosis

A 
disorder in epithelial transport affecting fluid secretion in exocrine glands & epithelial lining of respiratory, GI & reproductive tracts
-autosomal recessive
-dysfunction of CFTR gene
alteration in Cl & water transport 
-depleted fat stores & steatorrhea
183
Q

Define diffuse interstitial pulmonary fibrosis

A

unknown cause
inflammation, fibrosis & destruction..restrictive disease
honeycomb appearance of lung

184
Q

What is the hallmark of sarcoidosis?

A

noncaseating granulomas
Highest in N American blacks & females
loss of immune response, CNS may be affected

diagnosis of exclision

185
Q

Define pneumoconiosis

A

occupational lung disease caused by inhalation of particles

186
Q

Define Silicosis

A

occupational lung disease caused by inhalation of silicone

187
Q

Define asbestosis

A

occupational lung disease caused by inhalation of asbestos

188
Q

What are lung issues related to obesity?

A
  1. Reduced ventilatory drive
  2. Inc. workload of breathing
  3. Inc. abdominal girth can exert upward pressure on thorax
  4. Sleep apnea
189
Q

What are the types of pneumonia?

A 
inflammatory rxn in alveoli & interstitium
1. Community acquired
2. Hospital acquired 
3. Bacterial
4. Atypical
5. Viral
can be in bronchi/lobes
190
Q

What causes pernicious anemia?

A

Lack of intrinsic factor, a substance normally produced in the stomach that enables absorption of vitamin B12

191
Q

What is the erythron?

A

blood described as a single body system

192
Q

Anemia of chronic renal failure is caused by a lack of __________

A

erythropoeitin

193
Q

What cofactors are required for RBC production?

A
  1. Vitamin B12
  2. Folate
  3. Iron
194
Q

What forms of anemia will present w/ macrocytes?

A

Vitamin B12 & folate deficiency

195
Q

What is the major determinant of diastolic blood pressure?

A

systemic vascular resistance

196
Q

Which receptor is responsible for the innervation of the arterioles?

A

alpha-1

causes vasoconstriction & increased systemic vascular resistance

197
Q

The layer of squamous cells that lines the cardiac chambers and valves is called the __

A

endocardium

198
Q

Which nerve supplies the AV node?

A

the left vagus nerve

parasympathetic nerves stimulate a reduction in HR

199
Q

What portion of the heart does the left anterior descending branch supply?

A

apical & anterior

200
Q

The primary cause of sudden cardiac death is usually due to _______

A

Ventricular dysrhythmia

201
Q

What factor causes a congenital heart disease to produce cyanosis?

A

Right to Left shunting of blood

202
Q

What is the primary cause of airway obstruction in patients with chronic bronchitis?

A

mucus plugs

203
Q

What is the most common genetic CV disease?

A

Hypertrophic cardiomyopathy

Genetic mutation in sarcomeric proteins

IMS Exam 2 (1 decks)

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