P1 A&p Exam Final Redo

Front 1

1. Describe the functions of the cardiovascular system in maintaining homeostasis.

Back 1

Transporting materials from one part of the body to another.

Front 2

2. Define the terms blood pressure (BP) systolic and diastolic pressure.

Back 2

BP- pressure that moves blood through the body.
Systolic- ventricles contract (highest arterial) Generates Pressure
Diastolic- Ventricles relax (lowest arterial pressure.) Elastic properties help maintain this.

Front 3

3. Describe the role of pressure in the cardiovascular system.

Back 3

Pressure move blood through the body.

Front 4

 Where is the highest and lowest pressure?

Back 4

 Highest systemic Circulation 120/80 (normal)
 Lowest Pulmonary Cirulation 25/10 (normal)
 Generally pressure is highest near the heart and in arteries and lowers as you move further from the heart and into viens

Front 5

4. Describe the pulmonary circulation.

Back 5

Blood flows from the right atrium-> tricuspid valve-> right ventricle ->pulmonary semilunar valve->pulmonary Trunk-> lungs->pulmonary viens->left atrium

Front 6

 Which artery transports all the pulmonary blood?

Back 6

 Pulmonary Trunk

Front 7

 What is the pulmonary arterial systolic pressure?

Back 7

25 mm Hg

Front 8

 Which veins transport the pulmonary blood back to the heart

Back 8

 Pulmonary Veins

Front 9

 What net gas transport occurs in the pulmonary capillaries?

Back 9

CO2 out O2 in

Front 10

5. Describe the systemic circulation.

Back 10

Left atrium-> Bicuspid(mitral) valve-> left ventrical-> aortic semilunar valve->aorta-> systemic circulation->right atrium

Front 11

 Which artery transports all the systemic blood?
 What is the systemic arterial systolic pressure?

Back 11

 Arota
120 mm Hg

Front 12

 Which veins transport the systemic blood back to the heart
 What net gas transport occurs in the systemic capillaries?

Back 12

 Superior/inferior vena cava, Coronary sinus
In capillaries 02 is relases from blood CO2 is taken in.

Front 13

6. Contrast the pulmonary circulation & the systemic circulation in respect to blood pressure, cardiac output (CO), and resistance (R).

Back 13

Pulmonary circ is has less (R ) than Systemic circulation.
Cardiac output is the same for both.

Formulas
CO= SV x HR
CO= (EDV-ESV) x HR
CO= (120ml-50ml) x 75 bpm
CO= 5,250 ml/min

Front 14

7. Name the 4 chambers of the heart and describe their function.

Back 14

Left/Right Atrium, Left/Right Ventricle

Front 15

 Which 3 veins empty into the right atrium?
 Which 4 veins empty into the left atrium?

Back 15

Superior/Inferior Vena Cava, Corinary Sinus
4 Pulmonary Veins

Front 16

8. Define systolic and diastolic pressure.

Back 16

Systolic-Ventricular Contraction
Diastolic- Ventricular Relaxation

Front 17

9. Name the 4 valves of the heart and describe their function.

Back 17

Tricuspid valve- prevent backfrow from right ventricle to right atrium
Bicuspid (mitral) valve- “ “ from left ventricle to left atrium
Pulmonary Semilunar Valve- “ “ from Pumonary trunk to right ventricle
Aortic Semilunar valve- “ “ from Aorta to left ventricle

Front 18

 Which valve helps maintain pulmonary diastolic blood pressure?

Back 18

Pulmonary Semilunar Valve

Front 19

 Where is the tricuspid valve? What is the function of the tricuspid valve?

Back 19

 Between Right Atrium and R ventricle. Prevent backflow

Front 20

 When are the AV valves open? Closed?

Back 20

AV valves open when Pressure Atrium > Pventricles
Closed when Pventricle > Patrium

Front 21

 When are the semilunar valves open? Closed?

Back 21

 Open when Pventricle > Partery
 Closed when Partery > Pventricle

Front 22

10. Describe the role of pressure in the cardiovascular system.

Back 22

Pressure is what moves the blood through circulation

Front 23

 Where is the highest and lowest pressure?

Back 23

 Systemic artery circulation is the highest 120/80
 Pulminary circulation is Lowest 25/10
 Maybe higher or lower each vein and artery has its own BP

Front 24

11. Define the terms blood pressure (BP), stroke volume (SV), cardiac output (CO), resistance (R), and total peripheral resistance (TPR).

Back 24

Blood Pressure (BP)-Pressure excerted by circulation blood on vessel walls
Stroke Volume (SV)- Volume of blood pumped from one ventricle of the heart per contraction
Cardiac Output (CO)- Volume of blood being pumped by a ventricle per minute (SV x HR)
Resistance (R)- How easy or hard it flows
Total Peripheral Resistance (TPR)- Sum of the resistance of all the peripheral vasculator inn the systemic curcit.

Front 25

12. Describe the physical factors affecting resistance (R).

Back 25

Vessel length, diameter, blood composition etc

Front 26

1. Describe how cardiac muscle cell structure contributes to the specialized pumping function of the heart.

Back 26

Myo carium made up of branch cells (cardiac Myocytes) that have central nucleus. Joined together via intercalated discs ( special cell-cell connection has desmosomes to hold cells together with gap junctions to allow action potentials to go from cell to cell.) electrically myocytes behave as a single unit. Has Actin, Myosin, Myofilaments

Front 27

 How are cells coupled mechanically?
 How are cells coupled electrically?

Back 27

 Desmosomes
 Gap Junctions

Front 28

2. Describe the cardiac myocyte action potential and contrast it to skeletal and smooth muscle.

Back 28

-Cardiac Muscle
+ AP duration 200-400 ms
+Plateu from Ca current
+Refractory period as long as twitch-no tetany
+Mononucleated cells attached via intercolated disk
+Autorythmic
-Skeletal Muscle
+AP duration 1-10 ms
+Multiple AP can increase strength of contract produce tetany
+Multinucleated muscle fibers

Front 29

 What is the % calcium that enters the cytoplasm from extracellular fluid for each muscle type?

Back 29

 Skeletal ~1%
Cardiac ~10%
Smooth ~50%

Front 30

 Which muscle type would be most affected by calcium channel blockers?

Back 30

 Smooth muscles, they receive 50% Ca from ECF

Front 31

3. Define threshold potential, action potential and refractory period.

Back 31

Threshold Potential- Potential to with the membrane must depolarize to to start AP. Where voltage gated Na channels open

Front 32

4. Describe the movement of ions during the cardiac myocyte action potential.

Back 32

Na enters cell (depolarization)
Ca enters cell (Plateau Phase)
K Leaves Cell (repolarization)

Front 33

 What are L channels?

Back 33

 Long lasting high voltage activated Ca channels
Plateau Phase of all myocytes
AP of Pacemaker cells
Blocked by Ca channel antagonist
+Verapamil, Nifedipine, Nimodipine, and Diltazem

Front 34

5. List the various functions of calcium in myocyte excitation, contraction & relaxation.

Back 34

Ca voltage gated channels open
Ca enters cell triggers release of Ca from Sarcoplasmic Reticulum(ryanodine receptor RYR2-heart)
Binds to troponin & allows myosin to interact wit actin
Ca pumped out into SR and Out of cell
Relaxation happens when Ca unbinds from troponin

Front 35

 What is troponin?

Back 35

 Regulatory protein complex in all striated muscle.
3 subunits
+C (ca binding) unit- 1 gene
+I (inhibitory unit- 3 genes
-Fast skeletal muscle
-Slow skeletal Muscle
-Cardiac
+T (tropomyosin binding) Unit- 1 gene, 48 mRNA’s from alternate splicing w/ cardiac specific forms

Front 36

6. List the various cardiac myocyte functions that require ATP, and understand the requirement for oxygen.

Back 36

-Require ATP
+Myosin ATPase
+SR Ca Pump/ATPase
+Na/K ATPase
-O2 is needed to produce ATP (Provided by Coronary Blood Supply

Front 37

 How does digoxin work?

Back 37

 Poisons Na/K ATPase. This causes Increased Na in the cell which decreases the function of Na/Ca antiporter to pump out Ca. The increase in cytoplasmic Ca increases contraction of the heart improves cardiac output

Front 38

 What is the difference in calcium transport for SR vs plasma membrane?

Back 38

 Plasma Membrane uses Na/Ca antiporter to transport Ca out of cytoplasm nto ECF
 Ca ATPase Pump Pumps Ca into SR

Front 39

 What is myosin?

Back 39

 Myosin Interacts with Actin and myosin produces contaction.

Front 40

 What is Na/K ATPase?

Back 40

 It pumps Na out and K in. it maintains [C] gradient as well as make ATP

Front 41

 What is the Frank-Starling mechanism?

Back 41

 Greater volume of blood entering the heart in Diastole greater ejected during systole

Front 42

1. Describe the cardiac pacemaker cell action potential and contrast it to the cardiac myocyte action potential.

Back 42

-Pacemaker
+Autorythmic and generate own AP based on leak channels
+Have Depolarizing Resting membrane potential
+Ca Channel AP
+K Channel Repolarize
-Myocytes
+Stable Resting Membrane Potential
+Na Channel AP
+Ca Channel Plateau Phase
+K Channel Repolarize

Front 43

 What are funny channels? L channels? T channels? Leak channels?

Back 43

 L-type(long lasting High voltage activated)
+Plateau Phase Myocyte
+AP of Pacemaker Cells
+blocked by Ca channel antagonist
T-type(Transient, Low voltage activated)
+Present in Conducting and Pacemaker cells
+Help Regulate Vascular tone, signal conducting and cardiac pacemaking
+T-type antagonist->Mibefradil(Posicor)
I¬¬f (Funny) Channels
+Permeable to Na and K
+Its Hyperpolarization-activated cyclc nucleotide channel (HCN)
+cAMP increases opening of If channels
+Catecholamines (E & NE) increase HR by stim cAMP product via Beta-1 adrenergic receptor-G Protein

Front 44

2. Describe the movement of ions during the cardiac pacemaker cell action potential

Back 44

-Depolarization
+If Channels
+T-Type Ca Channels
+Until threshold potential is reached
-AP
+L-type Ca channels open after threshold potential is reached
-Ion movent conducted via Gap Junctions Cell-Cell
-Repolarization
+High voltage gated K channels open

Front 45

3. List the types of calcium ion channels in the heart.

Back 45

If Channel
T-Type
L-Type
P/Q-Type
Ryanodine Receptor
Inostiol Triphosphate Receptor (IP3R)

Front 46

4. Describe how autonomic neurotransmitters regulate heart rate.

Back 46

-Sympathetic (Beta-1,2 adernergic)
+Increase HR (Via increase cAMP)
+Epi & NEpi
-Parasympathetic (muscarinic)
+Decrease HR
+AcetylCholine

Front 47

5. Trace the depolarization of the heart and understand why you start at the SA node.

Back 47

SA Node->Ap thru neighbor cells via Gap Junction->AP Blocked at CT tissue AV Valves-> Slowly thru AV node(allows atria to contract)-> AP down His and Purkje fibers from apex upward.

Front 48

6. Explain the importance of the AV node in heart function.

Back 48

It slow the action potential giving the atrium time to contract before the ventricles begin to contract.

Front 49

7. Define tachycardia, bradycardia, complete heart block, SA node block, inotropic, chronotropic, and dromotropic.

Back 49

-Tachycardia- increased HR above 100 bpm
-Bradycardia- decreased HR below 60 bpm
-Complete Heart Block- AP stops at AV node no ventricle contraction (aka Third degree AV block) or damage His fiber ventricle will beat at a rate of Purkinje fibers
-SA Node Block- Block of AP at SA Node. Absent P-Wave
-Inotropic- affects force of contraction
-Chronotropic- affects HR
-Dromotropic- affects conduction of impulses
-Ectotropic Focus- AV node beats faster than SA node( Ventriclar Tachycardia) inefficient pumping.

Front 50

8. Describe how norepinephrine affects adnelyate cyclase activity to produce positive inotropic and chronotropic actions on the heart (B1).

Back 50

NEpi stim Adenlyate cyclase increase amount cAMP which binds If Channels opening them, stims protein phosphorlaytion by cAMP dependent protein Kinase which opens Ca channels. The extra Ca binds troponin increasing force of contraction.

Front 51

 What affect does the 1-adrenergic receptor associated G-protein have on adenylate cyclase?

Back 51

 Stimulates

Front 52

 What does cAMP do?

Back 52

Binds/Opens If Channels
Stim Protein Phosphorylation by PKA

Front 53

 What does PKA do?

Back 53

 Phosphorylates Phospholamban-P (increase SR Ca pump/ATPase dcreasing Ca

Front 54

 What does NE do to the pacemaker potential?

Back 54

 It increase HR by increase rate to threshold potential

Front 55

 How are troponin and ‘funny’ channels affected?

Back 55

up regultion in presence of cAMP

Front 56

9. Describe how the parasympathetic nervous system decreases blood pressure by decreasing cardiac output (muscarinic).

Back 56

It decreased CO,HR, Force of contraction. It also relaxes Smoth muscle and Dialates Blood vessels

Front 57

10. Compare and contrast ECG and intracellular recording

Back 57

Intracelular shows a plateau where ECG does not. ECG is the total heart while Intracellular in a single cell.

Front 58

1. Describe the mechanical activity of the heart during the P wave, PR segment, QRS complex, ST segment, T wave, & TP interval.

Back 58

-P wave- Atria contract
-PR segment Atria finishing contract
-QRS ?
-ST- ventricles contract
-T wave- ?
-TP- ventricles relax

Front 59

2. Define cardiac output, EDV, ESV, stroke volume, resistance, flow, isovolumic (isovolumetric) contraction, dicrotic notch, vasodilation and vasoconstriction.

Back 59

-CO- volume of blood pumped per minute
-EDV(End Diastolic Volume)- Volume of blood in ventricle before contraction
-ESV(End Systolic Volume)- Volume of blood in ventricle after contraction
-Stroke Voume- volume of bood moved by ventricle in one contraction
-Isovolumic (isovolumetric) Contraction- Q-T Interval contraction of heart
-Dicrotic Notch- the rise in the graph that represents the transient increase in arotic pressure
-vasodialation- blood vessels relax, get larger ( don’t know this by now you fail)
-Vasoconstriction- blood vessel diameter gets smaller

Front 60

3. Calculate cardiac output given EDV, ESV, and heart rate.

Back 60

CO=(EDV-ESV) x HR

Front 61

4. Describe how heart rate, preload and afterload will affect cardiac output.

Back 61

-HR
+Increase HR increase CO
-Preload (EDV)
+increase preload increase CO
-Afterload (ESV)
+Increase afterload decrease CO

Front 62

 How will increased sympathetic activity affect cardiac output?

Back 62

Increase it by increase contraction force.

Front 63

1. Contrast intrinsic regulation of blood flow to tissue by local factors to the extrinsic regulation of blood flow by the nervous system.

Back 63

Local control of blood flow is regulated by the metabolic needs of the tissue
Extrinsic (nervous) control is responsible for routing blood and maintaining pressure

Front 64

 What chemicals produce vasodilation?

Back 64

 Adenosine
 Decrease O2, Increase CO2 ,H , &/or K
 Nitric Oxide (NO)
+Bradykinin (Via NO)
+Acetylcholine(Via NO)
 Histamine
 Prostacyclin
 Epi & NEpi ( when acts on Beta-2 receptors)
 Natriuretic Peptides ( ANP & BNP)
 Vasoactive Intestinal Peptide

Front 65

 What chemicals produce vasoconstriction?

Back 65

 NEpi & Epi ( apha-1 Receptor)
 Serotonin
 Thromboxane A2
 Substance P
 Endothelin
 Angiotensin II
 Vasopressin ( Anti-diuretic hormone)
 ATP

Front 66

2. Describe the rapid autonomic responses to changes in blood pressure (increases & decreases).

Back 66

-Increase BP
+Increased Parasympathetic
+Decreased Sympathetic
+Decrease HR & Myocardial Contractility ( decrease CO)
+Vasodialaton of resistant vessels( decreases TPR)
+ Vasodialtion of Veins ( Decrease venous return lowering CO)
-Decreased BP
+Increase Sympathetic
+Decrease Parasympathetic
+Vasoconstriction of resistant vessles in muscle, kidney, splanchnic beds, and skin
(IncreaseTPR)
+VasoConstriction off Veins (increase venous return increase CO)
+ Increase HR & increase Myocardial Contracition

Front 67

 Where are the mechanoreceptors (baroreceptors) & what do they detect?

Back 67

 Receptor that detects changes in Pressure specificly for us BP right now

Front 68

 How do the mechanoreceptors respond to an increase in blood pressure?

Back 68

-Mechanorecptors firing increases
-Depressor region activity of Medullary Vasomotor Center Increase
+Parasympathetic activity increases to heart (More Ach decrease in HR)
-Pressor region activity of Medullary Vasomotor Center Decreases
+Sympathetic activity to arterioles, veins, heart decrease (decreases TPR)
Less NEpi

Front 69

 Where is the cardiovascular regulatory center?

Back 69

 Medulla Oblongota

Front 70

3. Describe how arterial vasoconstriction affects total peripheral resistance & blood flow.

Back 70

Increases TPR and Decreases Flow

Front 71

4. Describe how the sympathetic nervous system increases blood pressure by increasing cardiac output ( inotropic  chronotropic  dromotropic  venous return) and increasing total peripheral resistance.

Back 71

It increases the HR, & myocardial contractility. Causes Vasoconstricion to increase TPR & venous return (which increase CO)

Front 72

 What neurotransmitter causes the sympathetic effects on the heart?

Back 72

 Epi & NEpi ,

Front 73

 What neurotransmitter is released from the terminals of sympathetic pre-ganglionic neurons?

Back 73

 Ach

Front 74

 What neurotransmitter is released from the terminals of sympathetic post-ganglionic neurons?

Back 74

 Epi & NEpi

Front 75

 What type of neurotransmitter receptors is on the cell bodies of sympathetic post-ganglionic neurons?

Back 75

Nicotinic cholinergic receptors

Front 76

 What type of neurotransmitter receptors are on the cells of the heart?

Back 76

 Alpha & Beta Adrenergic receptors

Front 77

5. Describe how norepinephrine affects adnelyate cyclase activity to produce inotropic and chronotropic actions on the heart (1).

Back 77

Stimulates Adnelyate Cyclase to increase cAMP

Front 78

6. Describe how norepinephrine affects Phospholipase C activity to produce vasoconstriction (1)

Back 78

Increases it

Front 79

7. Describe how norepinephrine affects adnelyate cyclase activity to produce vascular smooth muscle relaxation (vasodilation) (2).

Back 79

increase it to rise cAMP levels

Front 80

8. Explain why an injection of epinephrine can increase cardiac output more effectively than norepinephrine.

Back 80

More affinity for beta-1 receptors

Front 81

 What will NE do to TPR?

Back 81

If it binds Beta-1 it decrease TPR
Binds Alpha-1 increase TPR

Front 82

 At low doses will NE stimulate alpha 1 or beta 2 receptors?

Back 82

alpja first then beta

Front 83

9. Discuss how decreasing venous compliance (increasing vascular smooth muscle tone) increases cardiac preloading.

Back 83

Compliance is basically the blood vessel wal stretch. Greater the venous compliance more blood in the veins. By decreaseing compliance your constricting smooth muscle, this increases BP which increases preload

Front 84

10. Describe how the parasympathetic nervous system decreases blood pressure by decreasing cardiac output (muscarinic).

Back 84

Ach released will decrease HR and contraction strength. Parasympathetic system also causes vasodialation which decreases preloading.

Front 85

 What neurotransmitter causes the parasympathetic effects on the heart?

Back 85

 Ach

Front 86

 What neurotransmitter is released from the terminals of parasympathetic pre-ganglionic neurons?

Back 86

 Ach

Front 87

 What type of neurotransmitter receptor is on the cell bodies of parasympathetic post-ganglionic neurons?

Back 87

Nicotinic Cholinergic Receptor

Front 88

 What type of neurotransmitter receptors are on the cells of the heart?

Back 88

Muscurnic

Front 89

 Which nerve carries parasympathetic input to the heart?

Back 89

 Vagus Nerve

Front 90

11. Describe the role of RAAS, vasopressin, & ANP in the long-term regulation of blood pressure/volume.

Back 90

-RAAS-(Renin Angiotensin Aldosterone System) increases Na/H2O reabsorbtion
(Increases Blood volume) as well as cause vasoconstriction
-VAssopressin-(ADH, Anti-Diuretic Hormone, or AVH)- increases BP and Blood
Volume by increasing water reabsorption and causing vasoconstriction
-ANP-(Atrial Natriuretic Peptide)-Inhibits release of ADH & Aldosterone, Causes
vasodialtion, stim urine producton which dcrease BP & Blood Volume.

Front 91

 What is renin?

Back 91

 Proteolytic enzyme released from juxtaglomerular cells kidney
 Cleaves Angiotensinogen to Angiotensin-I

Front 92

 What is angiotensinogen?

Back 92

Zyomgen that is cleaved by Renin to produce Angiotensin-I which is successively cleaved by ACE to angiotensin-II, Then III

Front 93

 What is ACE and what does it produce?

Back 93

 Angiotensin Converting Enzyme. Removes 2 AA from Angiotensin-I to make Angiotensin-II then cleaves II to make Angiotensin-III

Front 94

 What are angiotensin-II effects on blood vessels?

Back 94

Causes Vasoconsrtiction

Front 95

 What are angiotensin-II effects on the adrenal cortex?

Back 95

 Stimulates Aldosterone Production

Front 96

 What is aldosterone and where is it produced?

Back 96

Mineralocorticoid produced by cortex of the Adrenal Gland

Front 97

 What are aldosterone’s effects on the kidney?

Back 97

 Increase Na reabsorption in distal tubule and collecting duct
 H2O, Cl, Bicarb follow Na(water retention)
 Promotes excretion of K and H

Front 98

 What is ADH and where is it produced?

Back 98

-(Vasopressin)- RER of Magnicellular Neurons in Hypothalamus
-ADH release Stimulated by Increased ECF Osmoarity, Angiotensin-II,
Dcreased ECF Volume,and Decrease BP
-ADH release Inhibited by ANP and Ethanol

Front 99

 What are vasopressin’s effects on the kidney? on blood vessels?

Back 99

 Kidney- Via G-protein it increase Adenylate Cyclase-.Increases cAMP->PKA->Causes Aquaporin Insertion-> increases water reabsorption
 Ultimately it Increases Blood Volume via water reabsorption in kidney
 Blood Vessels- Via G-Protein-> PLC-> DAG & IP3-. Increases cycsolic Ca-.vasoconsrtiction
 Ultimately it Increases BP by causing Vasocontriction

Front 100

 What is ANP (and BNP) and where is it produced?

Back 100

ANP (arterial Natriuretic peptide) Cardiac Mucle of the Atrium
BNP (Brain Natriuretic Peptide) Produced by Ventricle muscle
ANP is released when Atrial BP is Increased ( BNP Too)

Front 101

 What are ANP’s effects on the kidney? on blood vessels?

Back 101

 Kidney- Stimulate urine output (inhibits ADH & ALdosterone)
 Blood Vessels- Vasodialation

Front 102

 What stimulates and inhibits the release of each of these hormones?

Back 102

 Renin
 +Stimulates
 -Decreased BP
 +Inhibtor
 -Increased BP
 Angiotensin-I,II
 +Stimulates
 -Renin (forms angiotensin-I)
 -ACE (Forms Angiotensin-II)
 +Inhibtor
 -Increased BP
 Aldosterone
 +Simulates
 -Angiotensin-II
 -Increased Potassium Levels
 -Ach(minor)
 -Dcreased Plasma Na
 +Inhibitors
 -ANP
 -Dopamine
 ADH (Vasopressin)
 +Stimulated
 -Increase ECF osmolarity
 -Angiotensin-II
 -Decrease in Blood Volume
 -Decrease in BP
 +inhibitors
 -ANP
 -Ethanol
 ANP
 +Stimulates
 -Atrial BP increases
 +Inhibitor
 -Atrial BP decreases

Front 103

12. Define hypotension, hypertension, & shock.

Back 103

-Hypotension-Low BP (<100/60)
+ Orthostatic Hypotension- Mech of CV compensating for changes upon standing.
Not enough blood to brain.
-Shock- Inadequate blood flow to all tissues
-Circulatory Shock- Extreme prolonged hypertension
+Hypovolemic Shock- Caused by loss of blood volume
+Cardiogenic Shock- Decreased Cardiac Output
+Vasogenic Shock- Caused by wide spread vasodialation
=Anaphylactic Shock- Vasodialation caused by histamine release due to allergic
reaction
=Septic Shock- Vasodialtion caused by substance relaeased by infectious agent
+Neurogenic Shock-Widespread vaso dialation due to sever pain or injury
-Hypertension- High BP (stage-1 140/90)
+Primary (essential or Idiopathic) Hypertension- Used to describe hypertention when
exact cause is unknown.
+Secondary Hypertension- High BP is caused by an Identified Problem
+Cardiovascular Hypertension- Caused by Arterio/atherosclerosis increasing TPR
and dcreasing vascular compliance
+Renal Hypertension- Caused by kidney diease
+Endocrine Hypertension- Abnormal hormone production
=Causes Pheochromocytoma, Conn’s Syndrome(extra aldosterone)
+Neurogenic Hypertentsion- tumors or defects in BP regulation centers

Front 104

13. List the causes of shock

Back 104

BP decrease (vasodialation)
Blood Volume loss( extra peeing, bleeding etc)
Decreased CO (Myocardial infarction)
Allergic reaction
Infection
Increase PNS decreased SNS for a long time

Front 105

 What is the danger of dehydration?

Back 105

 Can go into Hypovolemic Shock

Front 106

 What is the danger of allergic drug reactions?

Back 106

 Anaphylaxsis- increased histamine produced lots vasodialation

Front 107

15. Describe how partial blockage of a renal artery can produce hypertension.

Back 107

Reduced blood flow increasea RAAS activity which increases blood volume and vasoconstriction

Front 108

16. Describe the major physiological actions of drugs used to treat hypertension.

Back 108

-Diuretics
-Aldosterone Receptor Blockers
-Beta Adrenergic Receptor Blockers
-Angiotensin Converting Enzyme inhibitor
-Angiotensin Receptor Blockers
-Calcium Channel Blockers
-Direct vasodialators
-othe adrenergic Agengts

Front 109

 How does diuresis decrease blood pressure?

Back 109

 Increased urination causes water loos thus decreasing blod volume

Front 110

 How do beta blockers decrease blood pressure?

Back 110

 Slows down HR and prevent Vasoconstriction

Front 111

 How do calcium antagonists decrease blood pressure?

Back 111

 Bind Ca Channel Proteins which decrease Ca levels causing Smooth muscle to relax (vasodialation). It also causes decreased depolarization at the SA node reducing HR

Front 112

 How do ACE inhibitors decrease blood pressure?

Back 112

 Prevent converson of angiotensin-I to II which blocks angiotensin-II effects which is Vaso Constriction and the release of Aldosterone.

Front 113

 How do angiotensen receptor blockers decrease blood pressure?

Back 113

 Stops vasoconstriction and release of aldosterone

Front 114

 How do aldosterone receptor blockers decrease blood pressure?

Back 114

 Pevents aldosterone from causing Na Reabsoption. Decreasing blood volume

Front 115

 How will BNP affect blood pressure?

Back 115

 Do the same thing as ANP but with less affinity. It causes the release of ANP