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physpharm final exam > physpharm_semester_2_20240426001353 > Flashcards

physpharm_semester_2_20240426001353 Flashcards

1
Q

Name the path of blood through the pulmonary circuit starting at the superior and inferior vena cava

A
  • superior/inferior vena cava
  • right atrium
  • tricuspid valve (right AV valve)
  • right ventricle
  • pulmonary valve
  • pulmonary artery
    -pulmonary capillaries (on alveoli)
    -pulmonary vein
  • left atrium
  • mitral valve (bicuspid)
  • left ventricle
  • aortic valve
  • aorta
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2
Q

What are the two types of Myocardial cells?

A
  • Contractile (Cardiomyocytes)
  • Nodal and Conducting
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3
Q

Nodal and Conducting Cells characteristics

A
  • self excitable (ability to generate action potentials)
  • minimal actin and myosin
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4
Q

What is the threshold for a nodal cell to conduct an action potential?

A

-40mV

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5
Q

Charge of the cell during 1)Depolarization and 2)Repolarization

A

Depolarization - cell is more positive than RMP
Repolarization - returns back to RMP

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6
Q

Main differences between action potentials in a neuron vs a nodal cell

A
  1. Neuron AP is generated and conducted much faster
  2. In depolarization of a neuron - Na+ rushes in
    In depolarization of a myocardial nodal cell - Na rushes in but then right when repolarization starts, Ca rushes in to hold contraction for a bit
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7
Q

What is considered to be the pacemaker of the heart?

A

SA Node (Sinoatrial node)
- in right atrium
- fastest to excite = generation of APs

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8
Q

What is the conducting system path for action propagation through the heart?

A

1) SA Node –> Atrial Muscle –> AV Node –> Bundle of His –> Left and Right bundle branches –> Purkinje fibres –> Ventricular Muscle

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9
Q

What is occurring in the heart during each phase of the PQRST cycle?

A

P - Atrial Depolarization
QRS - Ventricular depolarization
T - Ventricular repolarization

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10
Q

How are cardiomyocytes different than skeletal muscle?

A
  • Branched cells
  • Lots of Mitochondria
  • Electrically connected
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11
Q

How does a cardiomyocyte action potential that stimulates muscle contraction work?

A
  • Sodium enters, causing very rapid depolarization
  • Potassium gates open to start initial repolarization
  • Calcium gates open to cause the plateau and to cause contraction of muscle due to calcium induced calcium release in SR
  • longer contraction of muscle due to Ca gate staying open (plateau)
  • Calcium gates close, and repolarization occurs
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12
Q

What are the Cardiac Cycle phases?

A

1) Atrial systole
2) Isovolumetric ventricular systole - no blood ejection, ventricular pressure increasing but valves closed
3) Ventricular systole - blood ejected from ventricles
4) Isovolumetric ventricular diastole - contraction of ventricles stopped, AV valves still closed
5) Late ventricular diastole - AV valves open, volume increasing

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13
Q

What is the average number of APs and the average heart rate of a human?

A

AP - 100 per minute
Heart Rate
- 70/min for male
- 80/min for female

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14
Q

Cardiac Output = ?

A

Cardiac Output = Stroke Volume x Heart Rate

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15
Q

What is the average intrinsic rate of the SA Node?

A

100 AP/min

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16
Q

What is the average heart rate for the average human?

A

Males - 70 beats/min
Females - 80 beats/min

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17
Q

True/False - The parasympathetic nervous system is the rest and digest stimulus pathway of the body

A

True

Parasympathetic - Rest and Digest
Sympathetic - Fight or Flight

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18
Q

PNS molecule and receptor

A

Molecule - Acetylcholine (ACh) from the postganglionic neuron

Receptor - Muscarinic receptors

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19
Q

SNS molecule and receptor

A

Molecule- Norepinephrine (from postganglionic neuron) and Epinephrine (from adrenal medulla respectively)

Receptor - Beta 1 (B1) Adrenergic receptors

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20
Q

Where are the SNS and PNS receptors located in the heart?

A
  • the SA node, AV Node, and ventricular muscle
  • notably large amount of B1 adrenergic receptors in ventricular muscle
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21
Q

What do the muscarinic receptors do?

A
  • Increase K permeability
  • Decrease Na and Ca permeability
  • Result of this is that the stroke volume is lower due to weaker contractions
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22
Q

What do the Beta 1 adrenergic receptors do?

A
  • Increase Na and Ca permeability
  • Triggers pathway that opens SR Ca channels
  • Stronger contractions so larger stroke volumes
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23
Q

End Diastolic Volume

A

Amount of blood in ventricle after atrial systole before ventricular systole
- point at which volume of blood in the ventricle is the highest

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24
Q

End Systolic Volume

A

Amount of blood in ventricle after ventricular systole
- point at which volume of blood in ventricle is the lowest

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25
Q

Stroke Volume = ?

A

EDV - ESV

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26
Q

Factors controlling stroke volume

A

1) Autonomic Nervous System

2) Preload on Heart

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27
Q

How does the ANS control stroke volume?

A

SNS - higher stroke volume due to stronger contractions
PNS - lower stroke volume due to weaker contractions

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28
Q

How does preload on heart affect stroke volume?

A

Increase in Preload = Increased Stroke volume

  • Preload increase = EDV increase
  • EDV increase due to increased venous return
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29
Q

(Review) What is an agonist and antagonist?

A

Agonist - binds to receptor and has an effect on the cell

Antagonist - binds to receptor but has no effect on the cell

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30
Q

What is a cholinergic agonist?

A

Binds to and activates the muscarinic receptors
- elicits PNS effect on heart (slower HR)
- example: nicotine

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31
Q

What does an acetylcholinesterase inhibitor do?

A

Inhibits the enzyme acetylcholinesterase, which is supposed to break down acetylcholine

  • therefore, ACh is not broken down and PNS is active for longer
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32
Q

What is the effect of Anticholinergics (cholinergic antagonist)?

A
  • prevent Ach from binding to the muscarinic receptors
  • prevent PNS activation
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33
Q

What is the effect of adrenergic agonists?

A
  • bind to beta 1 adrenergic receptors (which are all GPCRs) which activates the SNS
  • quickens HR
  • example: EpiPen
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34
Q

What is the effect of adrenergic antagonists (Beta Blockers)?

A
  • prevent epinephrine and norepinephrine from binding to adrenergic beta 1 receptors
  • prevents heart rate from speeding up
  • beta blockers usually end in -olol
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35
Q

What is bradycardia?

A

Condition where the heart is beating too slow

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36
Q

Difference between first generation and second generation beta blockers

A

First generation - non-selective as to which beta 1 adrenergic receptors it binds to in the body

Second generation - cardioselective

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37
Q

What is a heart Arrhythmia?

A

A condition where the heart is beating too slow (bradycardia), too quickly (tachycardia), or irregularly (fibrillation)

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38
Q

3 types of arrhythmias

A
  • Supraventricular arrhythmias
  • Ventricular arrhythmias
  • Bradyarrhythmias
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39
Q

What are the two main reasons arrhythmias occur?

A
  • issue generating action potentials
  • issue conducting action potentials
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40
Q

3 main ways arrhythmias can be treated

A
  • Beta blockers
  • Channel Blockers (K, Ca, or Na)
  • Pacemakers
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41
Q

In what direction does blood flow in during circulation?

A

High pressure to low pressure

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42
Q

Organization of blood vessels in order from leaving the heart

A

Arteries - arterioles - capillaries - venules - veins

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43
Q

Characteristics of arteries

A
  • Large diameter
  • Thin walls (relative to the diameter)
  • Very elastic
  • Low resistance
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44
Q

Characteristics of arterioles

A
  • small diameter
  • thick walls (relative to the diameter)
  • lots of smooth muscle (innervated by SNS)
  • CONTROLS BLOOD FLOW
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45
Q

MAP = ?

A

TPR x CO

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46
Q

Characteristics of capillaries

A
  • one cell thick
  • extremely thin walls - allows for gas exchange (diffusion)
  • low blood pressure
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47
Q

Two types of capillaries

A
  • Continuous capillary (less permeable)
  • Fenestrated capillary (more permeable due to pores connecting it straight to the tissue)
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48
Q

What are Starling forces?

A
  • forces which dictate filtration and reabsorption in the capillaries
  • many different forces due to different molecules and gradients
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49
Q

What is edema?

A
  • swelling due to excess fluids accumulating in tissue
  • due to excess filtration from capillaries
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50
Q

Characteristics of veins

A
  • large diameter
  • very thin walls compared to diameter
  • very low blood pressure
  • smooth muscle innervated by SNS
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51
Q

What is the skeletal muscle pump in veins?

A
  • smooth muscle in veins constrict in order to bring blood back to the heart
  • special valves prevent back flow
  • SNS can cause these smooth muscles to contract faster/harder
52
Q

How does the SNS increase blood flow through venous return?

A
  • innervates smooth muscles in veins (alpha adrenergic receptors)
  • faster/stronger contractions = higher EDV (preload)
  • higher EDV = increased stroke volume = increase CO
53
Q

What are the three types of mechanisms used to regulate blood flow?

A
  • Neural mechanisms (SNS and PNS)
  • Humoral mechanisms (substances in blood)
  • Local (tissue environment)
54
Q

True/False - The PNS innervates blood vessels and slows blood flow using direct blood vessel control

A

False

  • Only SNS innervates blood vessels (alpha adrenergic receptors)
55
Q

What are 4 humoral molecules which regulate blood flow?

A

Vasoconstrictors (stimulus is a decrease in BP)
- ADH
- Angiotensin ll

Vasodilators (stimulus is an increase in BP)
- Atrial natriuretic peptide
- Histamine

56
Q

Can epinephrine cause vasoconstriction AND vasodilation?

A

Yes

Vasoconstriction - by binding to alpha adrenergic receptors on blood vessels

Vasodilation - by binding to Beta 2 adrenergic receptors on heart, increasing blood flow indirectly causing blood vessels to dilate due to increased blood flow

57
Q

The two local mechanisms that control blood flow

A

Myogenic Theory - increased blood pressure means arterioles stretch, so arterioles contract back after stretching to original state or smaller to control blood flow

Metabolite Theory - change in metabolic needs/metabolites in the blood = higher/lower blood flow

58
Q

What are the receptors which detect changes in MAP and send signals to the CV centre in the medulla called?

A
  • baroreceptors (mechanoreceptors)
59
Q

Where are the mechanoreceptors that regulate MAP located?

A
  • walls of aortic arch and the carotid arteries
60
Q

How does the nervous system adjust the MAP when the it decreases?

A
  • SNS activation
  • heart pumps faster and harder = more CO
  • Blood vessels constrict = higher TPR
61
Q

How does the nervous system adjust the MAP when it increases?

A
  • PNS activation
  • Heart pumps slower and weaker = lower CO
  • PNS activated = no SNS activation on vessels meaning vasodilation = lower TPR
62
Q

What is hypertension?

A
  • high blood pressure
    Blood pressure >140 mm Hg
63
Q

Targets for treating hypertension

A
  • lowering TPR
  • lowering CO
64
Q

Treatments for hypertension

A
  • beta blockers (block SNS activity on heart)
  • Calcium channel blockers
  • Angiotensin-converting enzyme inhibitors (ACE inhibitors)
  • Angiotensin ll receptor blockers (ARBs)
65
Q

How do calcium channel blockers help treating hypertension?

A
  • Calcium channel blockers block calcium from entering smooth muscle on arteries = no vasoconstriction and decreased BP
66
Q

How do ACE inhibitors help treat hypertension?

A
  • prevents angiotensin l going to angiotensin ll
  • angiotensin ll leads to high BP by narrowing vessels
  • angiotensin 2 stimulates aldosterone production which increases blood pressure
  • therefore, stopping this reaction from taking place will decrease BP
67
Q

What are the two types of calcium channel blockers?

A
  • dihydropyridines (less effect on heart) and non-dihydropyridines (more effect on heart)
68
Q

How do angiotensin receptor blockers help treat hypertension?

A
  • blocks angiotensin ll from binding to its receptor
  • usually, angiotensin ll binding to the receptor causes vasoconstriction, so stopping that from happening will lower blood pressure
69
Q

What are the three mechanisms of hemostasis?

A
  • vasoconstriction around site of injury
  • platelet aggregation to stop bleeding (primary hemostasis)
  • coagulation cascade to form stable blood clot (secondary hemostasis)
70
Q

Why do platelets aggregate at a site of injury?

A
  • platelets adhere to collagen, which is exposed when a vessel is injured
  • when platelets contact collagen, they become active, sending chemical mediators (important one is called thromboxane) to recruit other platelets to the site of injury
71
Q

What is the final and most important product of the coagulation cascade?

72
Q

How can aspirin prevent a heart attack or a dangerous blood clot?

A
  • aspiring blocks enzyme responsible for release of thromboxane
  • results in less platelets activated and congregated
  • smaller/no blood clot formed
73
Q

What is Warfarin?

A

-Vitamin K important for synthesis of some clotting factors
- antagonist drug for vitamin K
- therefore, it stops clotting by blocking vitamin K from binding to receptors, inhibiting clotting to continue

74
Q

What is the functional unit of the kidney?

A

-The nephron

75
Q

Two major structures of the nephron

A
  • Renal corpuscle (where filtration of blood occurs)
  • Tubule (where the filtered fluid is processed)
76
Q

Main 5 parts of the nephron

A
  • renal corpuscle
  • proximal tubule
  • Loop of Henle
  • distal convoluted tubule
  • collecting duct
77
Q

Two types of nephrons

A
  • Cortical nephrons (in cortex)
  • Juxtamedullary nephrons (very close to medulla but still in cortex) - help in ability to produce more concentrated urine
78
Q

What is the site of filtration of blood that produces filtrate?

A

Renal Corpuscle

79
Q

Parts of the Renal Corpuscle

A

Bowman’s capsule - where fluid filters into
Glomerulus - specialized leaky capillaries
Juxtaglomerular apparatus - junction of the tubule and arterioles around Bowman’s capsule

80
Q

Which arteriole enters the renal corpuscle and which arteriole leaves it?

A
  • enters corpuscle - afferent arteriole
  • leaves corpuscle - efferent arteriole

TRICK TO REMEMBER- A COMES BEFORE E (A IS ENTERING, E IS LEAVING)

81
Q

What are the cells that wrap around the glomerulus call and what do they do?

A
  • called podocytes
  • fusion of podocytes to glomerulus due to sticky basal lamina
  • podocytes prevent filtration of larger molecules from blood
82
Q

3 Barriers to filtration

A
  • size of the pores in capillaries
  • space between the basal lamina matrix
  • slit space between podocytes
83
Q

What molecules are filtered into Bowman’s Capsule from the glomerulus? (5)

A
  • water, amino acids, glucose, ions, gases
84
Q

3 Processes that occur in the kidney

A
  • filtration (fluid from blood in glomerulus into Bowman’s capsule)
  • tubular reabsorption
  • tubular secretion
85
Q

What is the sum of all the forces in the renal corpuscle called?

A

Net Filtration Pressure

86
Q

The 4 Pressures affecting glomerular filtration (HCHC)

A
  • Hydrostatic pressure of glomerular capillaries
  • Colloid osmotic pressure of glomerular capillaries
  • Hydrostatic pressure of Bowman’s capsule
  • Colloid osmotic pressure of Bowman’s capsule
87
Q

What is the hydrostatic pressure of glomerular capillaries (Pgc)?

A
  • pressure cause by blood flowing into the glomerulus
  • promotes filtration
    ~55mm Hg
88
Q

What is the colloid osmotic pressure of glomerular capillaries(πgc)?

A
  • pressure caused by the presence of proteins in the glomerulus (in the blood)
  • inhibits filtration (osmosis)
    ~ 30mm Hg
89
Q

What is the hydrostatic pressure of Bowman’s capsule (Pbc)?

A
  • pressure caused by filtrate remaining in the Bowman’s capsule
  • inhibits filtration
    ~ 15 mm Hg
90
Q

What is the colloid osmotic pressure of Bowman’s capsule (π bc)?

A
  • pressure caused by the proteins in Bowman’s capsule
  • promotes filtration
    ~ 0 mm Hg
91
Q

Net filtration pressure = ?

A

NFP = Pgc - (Pbc + πgc)
= 55 - (15 + 30)
= 10

92
Q

What is the glomerular filtration rate (GFR)?

A
  • amount of fluid filtered by the kidney in a day
  • average value of 180 L/day
93
Q

Factors affecting GFR

A
  • NFP
  • Filtration coefficient (affected by the spaces in between podocytes and integrity of basal lamina)
94
Q

Two autoregulatory mechanisms to keep GFR constant

A
  • the myogenic response
  • tubuloglomerular feedback
95
Q

How does the myogenic response work?

A
  • afferent arteriole stretches from higher blood pressure, causing stretch sensitive ion channels to open
  • smooth muscle cells depolarize and calcium channels open, causing contraction of smooth muscles and vasoconstriction of the arteriole
  • blood flow decreases in glomerulus
96
Q

How does tubuloglomerular feedback work?

A
  • macula densa cells sense increase in ions (Na and Cl) due to increased flow rate
  • paracrine signalling (adenosine) from these cells to afferent arteriole
  • afferent arteriole constricts, reducing hydrostatic pressure in glomerulus and lowering GFR
97
Q

GFR = ?

A

GFR = ([Substance] in urine x Urine Volume) / [Substance] in plasma

98
Q

What does the filtered load calculate?

A
  • how much of a substance is filtered into Bowman’s capsule in a day
99
Q

True/False - Everything that gets filtered into Bowman’s capsule and enters the tubule system is excreted from the body

A

False - Reabsorption and more secretion occurs in the tubule system

100
Q

What molecules are reabsorbed in the proximal convoluted tubule?

A
  • glucose
  • sodium
  • water
  • amino acids
101
Q

What is reabsorbed in the Descending Limb of the Loop of Henle?

102
Q

What is absorbed in the Thick Ascending Limb of the Loop of Henle?

A
  • Reabsorbs ions
  • Na, Ca, Mg, K, Cl
103
Q

What is absorbed in the Distal Convoluted Tubule?

104
Q

What is absorbed in the Collecting Duct?

A
  • reabsorbs water and ions if necessary
105
Q

Main types of transporters in the tubule

A
  • channels (aquaporins, sodium channels)
  • transporters (glucose transporter, sodium/glucose symporter, antiporters - sodium/hydrogen exchanger)
  • primary active transporter (sodium/potassium ATPase)
106
Q

What is diabetes mellitus?

A
  • high concentration of glucose in urine due to high concentration of glucose in plasma
  • tubule cannot absorb all the glucose
  • high concentration of glucose in urine = high volume of urine due to osmosis
107
Q

True/False - Most drugs that are filtered into Bowman’s capsule due to not being bound to proteins are reabsorbed in the tubule system

A

False - most drugs that enter the tubule system are not reabsorbed

108
Q

What part of the tubule has many drug transporters which allows for selective secretion of drugs from the blood?

A

The proximal tubule

109
Q

True/False - Water balance and salt balance work in tandem and are controlled together.

A

False - Water and salt balance are controlled independently of each other

110
Q

If total body water decreases, what happens to the extracellular fluid volume and blood pressure?

A
  • Extracellular fluid volume decreases
  • blood pressure decreases
111
Q

What is ADH?

A
  • Also called Vasopressin
  • made in hypothalamus
  • stored in pituitary
  • peptide hormone
  • released due to high plasma osmolarity or low extracellular fluid volume
  • causes kidney to filter less water, so less water is excreted
112
Q

What receptors signal for ADH release?

A

Osmoreceptors (in hypothalamus) - senses increase in osmolarity in blood, so sends signal to release ADH

Baroreceptors - decrease in blood pressure leads to less action potentials being sent to hypothalamus - causes ADH to be released

113
Q

What does ADH actually do?

A
  • increases number of aquaporin ll channels on membrane of collecting duct
  • more water reabsorbed in collecting duct
114
Q

What is diuresis?

A
  • increased production of urine
115
Q

What is natriuresis?

A
  • increased excretion of sodium
116
Q

What is diabetes insipidus?

A
  • failure to release ADH (neurogenic) or failure of collecting duct cells to respond to ADH (nephrogenic)
117
Q

What do diuretics do?

A
  • inhibit ADH from binding to receptors (V2 receptors)
  • V2 receptor antagonists
118
Q

What are the two hormone systems that regulate body levels of sodium?

A
  • renin-angiotensin-aldosterone system (RAAS) - for when sodium is low
  • atrial natriuretic peptide (ANP) - when sodium is high
119
Q

What secretes renin?

A
  • juxtaglomerular cells
120
Q

Two receptor types that detect low sodium

A
  • baroreceptors - carotid sinus baroreceptors signal to JG cells (JG cells are also intrarenal baroreceptors)
  • chemoreceptors - Macula densa cells detect low Na and signal to JG cells through paracrine signalling
121
Q

What is angiotensin ll?

A
  • produced from angiotensin l
  • stimulus is renin release
  • causes increased reabsorption of Na in the proximal tubule
  • also causes vasoconstriction of the afferent and efferent arterioles, therefore decreasing GFR
122
Q

What is Aldosterone?

A
  • steroid hormone that increases reabsorption of Na and secretion of K in principal cells of the collecting duct
123
Q

What is the atrial natriuretic peptide (ANP)?

A
  • peptide hormone made by the atrial cells of the heart
  • stimulus is high blood pressure (will cause an increase in excretion of Na)
  • reduces reabsorption of Na by inhibiting aldosterone release and by vasodilation of the afferent arteriole
124
Q

What are the mechanisms used to treat high blood pressure?

A
  • reducing water absorption/increase water secretion (Diuretics)
  • reducing sodium reabsorption
125
Q

Types of Diuretics

A
  • V2 receptor antagonists (directly blocking ADH from binding to receptors)
  • NKCC2 antagonists (blocks NKCC2 symporter - therefore it prevents ion reabsorption)

NCC antagonists - blocks NCC symporter - therefore it decreases sodium reabsorption)

ACE inhibitors - prevents angiotensin l to ll conversion - therefore, prevents Na reabsorption and promotes vasodilation)

Angiotensin ll receptor blockers - prevents binding of Angiotensin ll to receptor - therefore, decreases sodium reabsorption

Aldosterone receptor blockers - block aldosterone from binding to receptor - therefore, reduces sodium reabsorption and prevents K secretion

Sodium channel blockers - inhibits epithelial sodium channels - therefore, reduces sodium reabsorption and prevents K secretion

physpharm final exam (32 decks)

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