Exam 3 Flashcards
(300 cards)
1
Q
Which of the following factors would decrease GFR?
A.A fall in plasma protein concentration (which decreases plasma oncotic pressure).
B.An obstruction such as a kidney stone in the tubular system (which increases Bowman’s capsule hydrostatic pressure).
C.Vasodilation of the afferent arterioles (which increases capillary blood pressure).
D.An increase in renal blood flow (which increases capillary blood pressure).
A
B.An obstruction such as a kidney stone in the tubular system (which increases Bowman’s capsule hydrostatic pressure).
2
Q
In the formation of urine, ___________ is a completely passive and non-selective process while _________ is selective and often requires the expenditure of energy.
A. Glomerular filtration, tubular reabsorption and secretion
B.Tubular reabsorption and secretion, Glomerular filtration
C.Sodium reabsorption, water reabsorption
D.Glucose reabsorption, sodium reabsorption
A
A. Glomerular filtration, tubular reabsorption and secretion
3
Q
When arterial blood pressure declines below normal, which of the following compensatory changes in renal function occur as a result of sympathetic nervous system activation?
A.Afferent arteriolar vasoconstriction B.Afferent arteriolar vasodilation C.Decreased Renin secretion D.Decreased ADH secretion E.None of the above
A
A.Afferent arteriolar vasoconstriction
4
Q
Below is a listing of nephron components and associated structures:
- Descending limb of loop of Henle
- Bowman’s capsule
- Collecting duct
- Ascending limb of loop of Henle
- Distal tubule
- Proximal tubule
Indicate the correct flow of fluid through these structures:
A
2, 6, 1, 4, 5, 3
5
Q
Which of the following statements about juxtamedullary nephrons is incorrect?
A.The glomeruli lie in the renal medulla.
B.Are important in the ability of the kidneys to concentrate urine.
C.The Loops of Henle span the entire depth of the renal medulla.
D.The vascular component contains a vasa recta.
E.Are not the predominant type of nephron found in human kidney
A
A.The glomeruli lie in the renal medulla.
6
Q
Which of your respiratory brain regions is NOT active during resting breathing?
A
Ventral respiratory group
7
Q
The purpose of the peripheral chemoreceptors is to sense changes in:
A.Plasma pH
B.PO2 of plasma
C.PCO2 of plasma
D.Both (a) and (b)
A
D.Both (a) and (b)
8
Q
Kussmal breathing is characterized by very deep and rapid respirations and is often seen with severe diabetic acidosis. In a patient experiencing diabetic acidosis, his/her _______ sense the fall in plasma pH and excites the medullary respiratory center to initiate Kussmal breathing which will, in turn, ________ to brings plasma pH back to normal.
A.Peripheral Chemoreceptors, lowers plasma PCO2
B.Central Chemoreceptors, lowers plasma PCO2
C.Central Chemoreceptors, elevates plasma PCO2
D.Peripheral Chemoreceptors, elevates plasma PCO2
A
A.Peripheral Chemoreceptors, lowers plasma PCO2
9
Q
Which of your respiratory brain regions (listed below) is NOT active during resting breathing?
A.Dorsal respiratory group
B.Ventral respiratory group
C.Pre-Botzinger complex
D.Pneumotaxic center
A
B.Ventral respiratory group
10
Q
Sarah has discovered a neat trick. She first holds her breath for as long as she can and takes note of that time. Next, she begins to breathe very rapidly with exaggerated exhalations for 30 seconds (i.e. hyperventilation). Finally, she holds her breath again for as long as she can and notices that she is able to hold her breath for nearly twice as long the first time. Why was Sarah was able to hold her breath longer the second time?
A
By hyperventilating, Sarah was able to lower her PCO2. This way when she held her breath the second time it took longer for her PCO2 to climb high enough to stimulate her chemoreceptors and force her to breath.
11
Q
In a healthy individual which of the following parameters is most important in regulating and maintaining normal respiration?
A.Plasma PO2
B.Plasma pH
C.Plasma PCO2
D.% Hb saturation
A
C.Plasma PCO2
12
Q
Which of the following would decrease the amount of gas diffusing from alveoli into the pulmonary capillary?
A.An increase in the thickness of the dissusion barrier
B.An increase in surface area available for diffusion
C.An increase in the partial pressure gradient
D.An increase in alveolar PO2
E.All of the above
A
A.An increase in the thickness of the dissusion barrier
13
Q
Which of the following would not result in lower oxygen saturation of hemoglobin?
A.A local increase in acidity
B.A local increase in temperature
C.A local increase in PO2
D.A local increase in PCO2
A
C.A local increase in PO2
14
Q
Normally, systemic venous PO2 is ________ alveolar PO2, and systemic venous PCO2 is ________ alveolar PCO2.
A.Greater than /// less than B.Less than /// equal to C.Equal to /// greater than D.Less than /// greater than E.equal to /// less than
A
D.Less than /// greater than
15
Q
The majority of CO2 in blood is transported (i.e. carried in blood) in which form?
A
As bicarbonate
16
Q
How is the majority of O2 carried by the blood stream?
A.Chemically bound to the heme groups on hemoglobin
B.Physically dissolved in plasma
C.In the form of bicarbonate
D.Chemically bound to the globin groups on hemoglobin
A
A.Chemically bound to the heme groups on hemoglobin
17
Q
Atmospheric air is composed mostly of:
A.Oxygen
B.Carbondioxide
C.Nitrogen
D.Water vapor
A
C.Nitrogen
18
Q
Select the incorrect statement about hemoglobin.
A.Its CO2 binding site is located at each heme group
B.It is located inside the red blood cell
C.Its globin portion is a polypeptide
D.It combines with oxygen at the lungs
E.It contains iron
A
A.Its CO2 binding site is located at each heme group
19
Q
The purpose of pulmonary surfactant is to:
A.Protect the alveoli from inhaled dust or debris
B.Remove water vapor in the alveoli
C.Prevent alveolar collapse
D.Increase the PCO2 in the alveoli
A
C.Prevent alveolar collapse
20
Q
Which of the following measures would apply to a patient with anemia (decreased red blood cell count – RBC count). Let’s say this person’s disease is severe enough that her RBC count is 10% less than normal?
A.arterial PO2 = 90mmHg
B.venous PCO2 = 30 mmHg
C.venous PO2 = 30 mmHg
D.arterial PO2 = 100mmHg
A
D.arterial PO2 = 100mmHg
21
Q
James is on a stationary bike at the gym. Imagine you were measuring the degree of oxygen extraction by all tissues in his body (i.e. how much O2 is taken out of blood by any tissue). You find that of all the tissue types in James’ body his oxygen extraction is highest in his quadricep muscles. Which of the following factors explains this finding?
A.The local temperture is higher in his quadricep muscle
B.The local pH is lower in his quadricep muscle
C.The local CO2 is higher in his quadricep muscle
D.All of the above
A
D.All of the above
22
Q
Which of the following will increase a person’s risk for Heart Failure?
A.A previous myocardial infarction
B.Left ventricular hypertrophy
C.Congenital or acquired defects in the cardiac conduction system
D.All of the above
A
D.All of the above
23
Q
With chronic heart failure the compensatory activation of the sympathetic nervous system causes increased heart rate, plasma volume expansion, and increased arterial blood pressure. How does this cause disease progression?
A.By increasing cardiac preload
B.By increasing afterload
C.By increasing cardiac O2 demands
D.All of the above
A
D.All of the above
24
Q
Which of the following measures total cardiac function and becomes inadequate with heart failure?
A.Heart Rate
B.Stroke Volume
C.Cardiac Output
D.Afterload
A
C.Cardiac Output
25
Left sided heart failure can directly lead to:
A.Dependent edema of the extremities
B.Liver congestion
C.GI distress
D.Pulmonary edema
D.Pulmonary edema
26
Which of the following drug types target the Renin-Angiotensin-Aldosterone system in the treatment of heart failure?
A.ACE-inhibitors
B.ARBs
C.Aldosterone antagonists
D.All of the above
D.All of the above
27
The progressive decline in cardiac output seen with chronic heart failure is a direct consequence of:
A.Increased production of Aldosterone
B.Peripheral vasocontriction
C.Cardiac remodeling
D.Plasma volume expansion
C.Cardiac remodeling
28
What is the primary rationale for the use of Beta Blockers to treat heart failure?
A.To reduce cardiac output
B.To reduce cardiac O2 demands
C.To prevent plasma volume expansion
D.To reduce cardiac preload
B.To reduce cardiac O2 demands
29
Right-sided heart failure can directly lead to:
A.decreased appetite and weight loss
B.Cough with frothy sputum
C.Activity intolerance related to decreased cardiac output
D.Pulmonary congestion
A.decreased appetite and weight loss
30
What is the primary rationale for the use of diuretics in the treatment of heart failure?
A.To reduce cardiac preload
B.To enhance cardiac output
C.To prevent cardaic remodeling
D.All of the above
A.To reduce cardiac preload
31
A patient with chronic anemia may develop chronic heart failure due to:
A.Compensatory plasma volume expansion
B.Chronic elevation in cardiac preload
C.Chronic elevation in afterload
D.All of the above
D.All of the above
32
Which of the following drugs is not commonly used to treat hypertension?
A.Diuretics
B.ACE inhibitors
C.digoxin
D.Beta Blockers
C.digoxin
33
Which of the following individuals would you expect is more likely to be hypertensive?
A.A 21 year man with a family history of hypertension.
B.A 35 year old woman who is obese, smokes and has diabetes.
C.An 75 year old man who is active, eats a healthy diet, is retired, and has no family history of hypertension.
D.A 25 year old woman who is overweight and has a family history of hypertension.
B.A 35 year old woman who is obese, smokes and has diabetes.
34
Which of the following etiologies is most common for hypertension?
A.Chronic renal failure
B.Idiopathic
C.Hyperaldosteronemia
D.Pregnancy
B.Idiopathic
35
Which of the following is (at least in part) directly responsible for the circadian influence over blood pressure.
A.The circadian changes in plasma concentration of cortisol
B.The circadian changes in the plasma concentration of growth hormone
C.The circadian changes in the plasma concentration of testosterone
D.The circadian changes in the plasma concentration of ADH
A.The circadian changes in plasma concentration of cortisol
36
Which of the following is normal, not pathological, and does not increase risk for pathology?
A.A night time drop in arterial blood pressure corresponding to sleeping hours.
B.An average daytime/waking blood pressure that equals average night time/sleeping blood pressure
C.A night time rise in arterial blood pressure corresponding to sleeping hours
D.An average daytime/waking blood pressure that is lower than average night time/sleeping blood pressure.
A.A night time drop in arterial blood pressure corresponding to sleeping hours.
37
Deficiencies in which of the following minerals/electrolytes increases a person's risk for hypertension?
A.Potassium
B.Sodium
C.Zinc
D.Chromium
A.Potassium
38
True or false: A diagnosis of hypertension requires both systolic and diastolic pressure to be persistently elevated.
False
39
African Americans have a higher risk for hypertension than other racial groups. Which of the following best describes the originating genetic vulnerability that underlies this enhanced risk?
A.A tendency toward increased vascular smooth muscle growth.
B.A tendency toward enhanced vascular responsiveness.
C.In adequate sodium excretion
D.A tendency toward a higher resting heart rate.
C.In adequate sodium excretion
40
Which of the following best describes the recommended first line intervention when treating a patient first diagnosed with hypertension?
A.The introduction of a low dose anti hypertensive drugs
B.The use of more than one anti hypertensive drugs to achieve adequate control
C.Lifestyle modification
D.None of the above
C.Lifestyle modification
41
True or false: A blood pressure reading of 120/80mmHg is common and considered optimal.
false
42
Which of the following lipoproteins is responsible for delivering cholesterol to tissues?
A.Chylomicrons
B.VLDLs
C.LDLs
D.HDLs
C.LDLs
43
In addition to there being an optimal total cholesterol count, the goal is often to achieve the lowest possible _______ count and the highest possible _______ count
A.LDL///HDL
B.HDL///LDL
C.HDL///triglyceride
D.Triglyceride///LDL
A.LDL///HDL
44
Lipoproteins that contain the greatest proportion of ______ tend to be greatest in density.
A.Triglycerides
B.Phospholipids
C.Protein
D.Cholesterol
C.Protein
45
Cells of which organ are responsible for taking up the greatest amount of LDLs from circulation via the receptor-dependent mechanism/pathway.
A.Adipose tissue
B.Adrenal cortex
C.Liver
D.Ovaries/testes
C.Liver
46
Which of the following lipoproteins is responsible for delivering triglycerides to tissues?
A.Chylomicrons
B.VLDLs
C.LDLs
D.HDLs
A.Chylomicrons
47
During exercise which of the following factors contributes to the increase in perfusion of active muscle?
A. Local decrease in CO2 production by active muscle
B. Local decrease in O2 consumption by active muscle
C. Increased arteriolar resistance to flow (locally supplying muscle)
D. Relaxation of precapillary sphincters (locally supplying muscle)
E.All of the above
D. Relaxation of precapillary sphincters (locally supplying muscle)
48
Imagine that you are treating a burn patient and his blood work shows a decreased serum albumin level. The inflammation and exposed burn wounds have led to an excessive loss of albumin. You also notice that he is suffering from generalized pitting edema. What explains the edema based on the above information regarding this patient?
Decreased plasma osmotic (colloid oncotic) pressure increases bulk flow out of capillaries and into interstitial space
49
Why is the baroreflex considered only a short term strategy for regulating Mean Arterial Blood Pressure?
A.Because drops in blood pressure sensed by the aortic and carotid baroreceptors cannot lead to an increase in Angiotensin II which is necessary to increase plasma volume
B.Because the aortic and carotid baroreceptors adapt to sustained changes in blood pressure
C.Because renal baroreceptors are more efficient at adjusting heart rate in response to sustained changes in blood pressure.
D.All of the above
B.Because the aortic and carotid baroreceptors adapt to sustained changes in blood pressure
50
Endothelial-derived relaxing factor (EDRF) is
A.Adenosine
B.Nitric Acid
C.Norepinephrine
D.Endothelin
B.Nitric Acid
51
The direction of the action potential movement through the conduction system of the heart for each cardiac cycle is normally
SA node—AV node—bundle of His—Purkinje fibers
52
Which of the following would cause an increase in Mean Arterial Pressure (either directly or indirectly)?
```
A.Increased ventricular filling
B.Increased venous return
C.Increased heart rate
D.Increased arteriolar vasoconstriction
E.All of the above
```
E.All of the above
53
Which of the following is not a factor that either enhances or contributes to maintaining venous return of blood to the heart?
A.High compliance of the venous system
B.Skeletal muscle contraction
C.cardiac suction
D.Venous valves
A.High compliance of the venous system
54
Which two pressures promote the bulk flow movement of fluid into the capillary?
Interstitial-fluid hydrostatic pressure and plasma oncotic pressure
55
Which of the following conditions can cause vasodilation of systemic arterioles?
```
A.High O2 concentrations
B.High pH
C. Low CO2 concentrations
D.High CO2 concentrations
E. All of the above
```
D.High CO2 concentrations
56
There are many factors that can damage the endothelial lining of blood vessels throughout the body including smoking, dislipidemia, uncontrolled diabetes, and hypertension. Patients with endothelial damage (and dysfunction) to the coronary arteries that perfuse the heart are at higher risk for cardiac ischemia (i.e. O2 deprivation). Why?
A.Because there is impaired endothelial sensitivity to local concentrations of O2, CO2, pH, and adenosine
B. Because there is impaired endothelial release of Nitric Oxide
C. Because local tissue perfusion is not being matched to metabolic need
D.All of the above
D.All of the above
57
why would a patient's venous blood not get cleared, causing sore on his leg?
venous stasis is a result of RIGHT-SIDED HEART FAILURE
58
What is a lipoprotein? What types of lipoprotein exist?
Lipoproteins are special fat-carrying proteins. There are five types of lipoproteins (classified by density):
1) Chylomicrons
2) Very-low density lipoproteins (VLDL)
3) Intermediate-density lipoproteins (IDL)
4) Low-density lipoproteins (LDL)
5) High-density lipoproteins (HDL)
59
What are the possible routes of elimination for LDLs in circulation?
receptor-mediated uptake: primary pathway used by the liver (also used by the adrenal cortex, testes, and ovaries) - in this method, receptors on tissue membranes uptake cholesterol in order to synthesize hormones etc.
reverse cholesterol transport: this is considered the “good” pathway - HDLs bind to the LDLs that are in circulation and get them returned to the liver
scavenger pathway: this way is damaging to the body - in this way, LDLs interact with reactive oxygen species in circulation and become “oxidized” and very reactive, so they damage the lining of blood vessels —> this leads to inflammatory response (release of cytokines, monocytes become macrohpages) and LDLs get consumed/removed by the macrophages in circulation
60
The majority of LDL receptors (75%) are found on the
liver—the liver primarily uses cholesterol to produce bile salts
61
What is HDL? Where does it come from? What role does it play in regulating circulating lipid levels? Why is it considered the “good” cholesterol?
HDL is part of our reverse cholesterol transport pathway (the “Good pathway”) - it’s the molecule that brings LDLs back to the liver.
Low levels of HDL means that the patient doesn’t necessarily have those protective enzymes - increase exercise, increase eating foods high in omega 3 fat acids
62
What is Primary hypercholesterolemia?
a genetic predisposition - it’s when elevated levels of cholesterol (namely LDLs) develop independently of other health problems or lifestyle behaviors.
63
Potential causes for Primary hypercholesterolemia?
often genetic, such as defective synthesis of apoproteins, lack of LDL receptors, defective LDL receptors, defective HLD enzymes
64
“Cheerios” claims to reduce cholesterol levels if eaten daily for at least a few weeks. By what mechanism is this accomplished?
Cheerios have Oat bran which is a water soluble fiber —> increasing water soluble fiber in your diet forms gooey substance in your intestines which will bind to bile salts and cause the bile salts to be excreted. When the bile salts are excreted, the liver makes more bile salts by taking up more LDLs from circulation, thereby reducing cholesterol levels (preventing the recycling of bile salts from your GI tract)
65
By what mechanism do the “Statin” class drugs lower cholesterol?
Most common pharmacological intervention is the use of statin drugs
Statins work by blocking the HMG CoA reductase inhibitors
HMG CoA reductase is the enzyme thats used by the liver to synthesize cholesterol
Therefore, statins inhibit this enzyme from working
66
What are the four requirements or steps to normal external respiration discussed in class?
Ventilation — Lungs
Gas exchange — Lungs -> Blood
Gas Transport— Blood
Tissue extraction/deposition — Blood —> Tissues/Cells
67
Hypoxia vs Hypoexmia
Hypoxia: deficiency of oxygen anywhere
Hypoexmia: deficiency of oxygen in the blood
68
Abnormal Ventilation pathological condition:
```
Pleural abnormalities
Pneumothorax
Open Pneumothorax
Tension pneumothorax
Spontaneous pneumothorax
Hemothorax (blood buildup in lungs)) or Pleural effusion (fluid buildup in lungs) — both would require chest tube for drainage
```
Restrictive Lung Disease
Obstructive Pulmonary disease
69
Abnormal Gas exchange pathological condition:
Adult Respiratory Distress (An explosive form of respiratory failure characterized by acute lung inflammation and diffuse alveolocapillary injury)
High Altitude – reduced atmospheric PO2
Pulmonary edema
Ventilation-Perfusion Mismatch
70
What is a Hemothorax
blood buildup in lungs
71
What is Adult Respiratory Distress
An explosive form of respiratory failure characterized by acute lung inflammation and diffuse alveolocapillary injury
72
Abnormal Gas Transport pathological condition:
Anemic Hypoxia
| CO poisoning
73
Abnormal Tissue Extraction/deposition/utilization of O2 pathological condition:
Histotoxic Hypoxia (cyanide poisoning)
74
What is a pneumothorax?
when the lung collapses and equalization of pressures (inside and outside of the lungs)
Once the lung is collapsed, it can NO LONGER INFLATE
75
Open pneumothorax
air can enter and leave pleural space (ex. penetrating chest wound)
76
Closed pneumothorax
air enters pleural space from lung and cannot escape
77
tension pneumothorax
air enters pleural space from outside or lung itself and cannot leave (often see tracheal deviation)
78
An open pneumothorax is associated with the rupture of which pleural membrane in the thoracic cavity?
In an open pneumothorax, there is injury to the chest wall and PARIETAL PLEURA membrane is ruptured in the pleural cavity
In an open pneumothorax, air can enter and leave the pleural space - equalization of pressures from outside and inside, lung can no longer inflate
Example: Penetrating chest wound, gunshot
79
Rupture of which pleural membrane in the thoracic cavity causes a spontaneous pneumothorax?
Spontaneous pneumothorax is a type of CLOSED pneumothorax - the VISCERAL PLEURA is injured/broken
someone who may seemingly have no risk factors for a pneumothorax may spontaneously develop one (perhaps playing an instrument or some such)
in TENSION: both visceral and parietal membranes are ruptured
80
For someone suffering from CO poisoning what would you expect the status of each of the following parameters to be: PaO2, PaCO2, %Hb saturation measured by standard pulse oximetry, and skin color?
PaO2 = unchanged, still normal
PaCO2 = will be either normal or low
% Hb saturation measured by standard pulse oximetry = normal
Skin color = flushed or pink
81
What is residual volume? Is residual volume normal?
Residual volume is normal - it’s the amount of air remaining in the lungs after you exhale
82
What are FVC and FEV1? How does FEV1 relate to FVC in a normal healthy lung?
FVC = forced vital capacity
FEV1 = forced expiratory volume in 1 second
FEV1 will be approx 80% of FVC in a healthy individual
83
What are the most common types of obstructive lung diseases?
Asthma
Acute and Chronic Bronchitis
Emphysema
84
Obstructive Pulmonary Diseases Basic characteristics:
airway narrowing, air trapping, and expiratory wheezing
85
Etiologies for Asthma
Chronic inflammatory disorder is the underlying cause
Can be triggered by allergies/irritants, cold weather, emotion
86
Etiologies for Acute and Chronic Bronchitis
Inflammation
hyper secretion of mucus
ciliary malfunction
predisposed to bacterial colonization
exacerbated by irritants, pollution
87
Etiologies for Emphysema
Dilation of the alveolar sacs due to constant and reoccurring breakdown of lung tissue
Can come from smoking
There’s also a genetic predisposition: absence of Alpha 1 Tripsin
88
clinical manifestation of asthma
```
acute bronchospasm
fluid buildup in lungs
expiratory wheezing
dyspnea, SOB
using accessory muscles to breathe when having exacerbation
```
89
clinical manifestation of Acute and Chronic Bronchitis
dyspnea, SOB, cough
pulmonary secretions
severe: hypercapnia (increased CO2 in blood) and hypoxemia (decreased O2 in blood)
90
treatment for asthma
Albuterol (rescue treatment - short acting beta 2 agonist)
Inhaled corticosteroid for more severe - this is a daily med to treat underlying chronic inflammation
91
treatment for Acute and Chronic Bronchitis
Smoking cessation
Lung rehabilitation/exercises
Albuterol (rescue treatment - short acting beta 2 agonist)
Inhaled corticosteroid for more severe - this is a daily med to treat underlying chronic inflammation
Some patients might be on long-term oxygen and/or anticholingerics to dry up the secretions
92
treatment for Emphysema
Smoking cessation
Lung transplant
Oxygen for symptom relief
medications for symptom relief
93
Cause and impact of Restrictive (Pulmonary Fibrosis, Infant Respiratory Distress Syndrome)? What is the effect on lung volume?
cause: Lung noncompliance
impact: Increased inspiratory effort
lung volume: decreased
94
Cause and impact of Obstructive (Asthma, COPD - Bronchitis and Emphysema)? What is the effect on lung volume?
cause: Narrowing of airways, air trapping
impact: Expiratory wheezing
lung volume: increased
95
Function testing for Restrictive (Pulmonary Fibrosis, Infant Respiratory Distress Syndrome)?
decreased inspiratory capacity
ratio of FEV1 (forced expiratory volume in 1 second)/FVC (forced vital capacity - the patient forcefully breathing out a full breath) not affected generally
96
Function testing for Obstructive (Asthma, COPD - Bronchitis and Emphysema)?
decreased inspiratory capacity
increased residual volume (amount of air left over in lungs after you’ve breathed out)
decreased ratio of FEV1/FVC
97
What cell types make up the interface between the alveoli and the pulmonary capillaries?
```
Type 1 alveolar cells (Pink wall)
Type 2 alveolar cells (blue cell)
Alveolar macrophage (yellow)
capillary endothelial cells
Erythrocytes (right sausage shape on right)
```
98
What do Type 1 alveolar cells do?
form the walls of the alveoli
99
What do Type 2 alveolar cells do?
produce surfactant – breaks up surface tension of water (from humid air) and helps prevent alveoli from collapsing
100
What do Alveolar macrophage cells do?
immune cells that phagocytizes debris/bacteria
101
What do capillary endothelial cells do?
form the walls of Pulmonary capillary
102
What do Erythrocytes do?
passing through pulmonary capillaries, where hemoglobin is located
103
Gas exchange is done by what type of diffusion?
passive
104
Surface area decreases (reduced functional alveoli) results in
decreased gas exchange
105
Thickness increases (scar tissue) results in
decreased gas exchange
106
Amount of gas transported =
(Surface area/thickness of diffusion barrier) x partial pressure gradient
107
What determines the % hemoglobin saturation?
PO2 of the plasma determines the hemoglobin saturation
108
Factors that affect % Hb saturation, makes hemoglobin more likely to unload O2:
CO2 concentration
Acidity
Temperature
Oxygen-hemoglobin dissociation curve
109
What are the ways in which O2 is transported in blood and in what proportions?
Physically dissolved in plasma – 1.5%
| Chemically bound to hemoglobin – 98%
110
What are the ways in which CO2 is transported in blood and in what proportions?
Physically dissolved in blood – 10%
Bound to hemoglobin – 30%
In the form of bicarbonate – 60%
111
What part of the medullary respiratory center gets recruited in forceful breathing?
Ventral group
112
What muscular events are involved in Quiet inhalation?
diaphragm (contract and flattens), external intercostals (contracts and lifts the rib cage)
113
What muscular events are involved in Forceful inhalation?
diaphragm (greater intensity), external intercostals (greater intensity), sternocleidomastoid and scalenus muscle (lift the sternum and clavicle)
114
What muscular events are involved in Passive exhalation?
passive, relaxes the diaphragm and external intercostals
115
What muscular events are involved in Forceful exhalation?
contracting abdominal muscles to push diaphragm up, contracting internal intercostal muscles to pull ribcage in and down
116
What part of the medullary respiratory center is responsible for driving quiet resting breathing?
Dorsal group is responsible for quiet, restful breathing, even responsible for forceful breathing but not maximal breathing, recruits ventral group for when you need accessory muscles on board
117
There is a term called Kussmal breathing that is characterized by very deep and rapid respirations and is often seen with severe diabetic acidosis (which is a metabolic acidosis – hint: caused by non-CO2 derived acidity). Based on what you know about respiratory control, what sensors stimulate this type of breathing? What is the purpose of Kussmal breathing in a patient with diabetic acidosis? Would you expect the systemic arterial PCO2 of this patient to be high, low, or normal?
Ketoacidosis – build up of ketones causes blood pH to be low/acidic, metabolic acidosis
The blood acidity is measured by the peripheral chemoreceptors.
Central chemoreceptors can only measure pH of CSF. They sense the acid in the blood and stimulate Kussmal breathing to blow off CO2 this promotes the reverse reaction (Bicarb (HCO3) (low) + H (high) H2CO3 (low) H2O + CO2 (low from Kussmal)) which takes H+ out and lowers acidity
PCO2 is normal at the beginning because respiratory system is not the problem, once Kussmal breathing starts it drops
118
Name two structures in the respiratory system that are considered to be “Anatomical Dead Space”. Why are all these structures considered Dead space?
Larynx, pharynx, trachea, bronchi, mouth, nose and sinuses
Basically anything from where enters to terminal bronchioles because there is no gas exchange going on there but you have to ventilate it
119
Sarah has discovered a neat trick. She first holds her breath for as long as she can and takes note of that time. Next, she begins to breathe very rapidly with exaggerated exhalations for 30 seconds. Finally, she holds her breath again for as long as she can and notices that she is able to hold her breath for nearly twice as long the first time. Briefly explain why Sarah was able to hold her breath longer the second time.
When she hyperventilates she lowers her PCO2 because she blows it off, so it takes longer for it to build up to the point where it forces her to breath
The central chemoreceptors trigger this because they are highly sensitive to changes in PCO2 because it diffuses across the blood brain barrier
120
What happens in Glomerular filtration
about 20% of the plasma that enters the glomerular capillaries will be filtered into bowman’s capsule
the other 80% moves on to the efferent arterioles and peritubular capillaries
passive, non-selective process
121
What happens in Tubular reabsorption?
when fluid/substances move from the tubule back to the blood/capillaries
sometimes active, sometimes passive
ALWAYS selective
122
What happens in Tubular secretion?
when substances move from the capillaries TO the tubule (something that didn’t get filtered that we want to add to the contents of urine)
mostly active, sometimes passive
ALWAYS selective
123
What are the forces involved in glomerular filtration?
Capillary blood pressure
Plasma Colloid Oncotic Pressure
Bowman’s Capsule Hydrostatic Pressure
124
What are the forces that promote filtration?
Capillary blood pressure (pushes blood out of glomerulus and into bowman’s capsule) - 55 mm Hg
125
What are the forces that oppose filtration?
Plasma Colloid Oncotic Pressure (pulling fluid from bowman’s capsule into the glomerulus) - 30 mm Hg
Bowman’s Capsule Hydrostatic Pressure (pushes fluid back into glomerulus) - 15 mm Hg
126
Net filtration pressure =
10 mm Hg
127
What is the goal of autoregulation by the kidneys? By what mechanisms is this goal met?
Goal is to maintain GFR in the face of normal fluctuations in blood pressure
How it’s met: the Juxtaglomerular apparatus
1. Change in BP
2. Change in BP is sensed by the macula dense cells
3. Maculadensa cells stimulate granula cells (lying on the afferent arteriole of the nephron)
4. Granula cells either cause vasoconstriction (decrease GFR) or vasodilation (increase GFR)
128
What are the structural and functional differences between the juxtamedullary nephrons and the cortical nephrons?
juxtamedullary nephrons = long, extend deeper into the medulla and originate in the cortex closer to medulla, make up 20% of our nephrons, has the Vasa Recta
cortical nephrons = short, make up 80% of our nephrons, short loops of Henle and lots of capillaries
both originate in cortex of kidney
129
Describe the vascular components of the nephron. Which vascular parts engage in exchange of any kind with the tubule?
Exchange with the tubule occurs at the glomerulus, peritubular capillaries, Vasa recta (if juxtamedullary nephrons)
130
Consider the Renal Corpuscle, how does it manage to filter out small proteins like albumin that can fit through the pores of the capillary walls?
Renal corpuscle is the glomerulus and Bowman’s capsule
the glomerular membrane, specifically the basement membrane (filters out albumin because its negatively charged - it repels proteins) and the inner layer of bowman’s capsule (filters out albumin based on size)
131
Which of the tubular segments is the only one where sodium is not reabsorbed?
Descending loop of Henle
132
Paracellular Route (in between epithelial cells) in the proximal tubule
leaky tight junctions
these junctions are “tight” – however, they are “leaky” enough to allow water through, leakiest are found in proximal tubule.
osmolarity is high—suck water in between the cells
driven by lateral spaces, and HYPERosmotic concentrations
133
Transcellular Route (through epithelial cells) in the proximal tubule
NO leaky tight junctions;
water movement requires aquaporins to get through both membranes; and osmotic gradient between tubular fluid and interstitial fluid.
Na+ moves in, increases osmolarity of the cell; water also moves in.
Note: Differences: permeability (aquaporins and leaky tight junctions) vs. driving force (osmotic gradient)
134
Explain how you know for certain that the kidneys do not regulate plasma levels of glucose.
Usually 100% of glucose is reabsorbed in prox. tubule and returned into bloodstream; if glucose is >375mg/min, it will be excreted in urine.
So, 100mg is normal for blood glucose, and 300 is renal threshold, (3x normal), blood glucose has to triple before kidneys stop reabsorbing, so because threshold is so much higher than normal range, they are not helping to regulate plasma glucose.
135
Explain how potassium secretion is linked to sodium reabsorption, but only in the distal tubule and collecting duct.
Potassium is actively secreted in distal tubule and collecting duct:
Aldosterone causes sodium retention (or enhances sodium reabsorption), which causes a LOSS of potassium.
The higher the aldosterone level, the more Na+ os reabsorbed, and therefore the more potassium is excreted.
136
What factors will determine if a segment of tubule is permeable to water?
ADH controls the amount of nephron segment that is permeable to water
137
The medullary osmotic gradient plays a key role in the kidneys ability to produce urine of varied concentrations. What structure (s) establishes this gradient and which structure (s) uses the gradient to vary the concentration of urine?
The long loops of Henle (of the Juxtamedullary nephrons) establish the osmotic gradient via the countercurrent system of the kidney - and the collecting duct uses this established gradient to vary the concentration of urine.
138
How is the medullary osmotic gradient used to vary the concentration of urine?
Urine concentrates going down the descending loop of henle (which is impermeable to Na, and thus stays in the renal tubule); urine dilutes as it goes up the ascending loop of henle (which is impermeable to water; water stays in the tubule while Na leaves). Thus, at the top of the collecting duct, urine is relatively dilute: around 100 mOsm. As this urine moves down the collecting duct, aquaporins allow movement of water out of the tubule, and subsequently allows H20 to be reabsorbed until it equilibrates w/ the interstitial fluid of the renal medulla (this is how the collecting duct uses the established gradient to vary the concentration of urine!)
139
What role does ADH play in concentration of urine?
The concentration of ADH in the blood determines how much of distal tubule and collecting duct is permeable to water.
140
Renal Threshold
the maximal plasma concentration of any organic nutrient can achieve before it starts to appear in urine.
141
Tubular Maximum:
the maximal rate of reabsorption; the point of saturation
142
How does the body regulate plasma volume? How does it regulate plasma osmolarity? Describe in terms of exact mechanism and explain how these systems intersect.
Essentially:
1. Blood pressure/fluid volume regulation: Baroreceptors are able to detect fluctuations in BP and allows the kidneys to regulate blood volume via the sympathetic N.S. and Renin Angiotensin Aldosterone System (RAAS).
2. Plasma osmolarity regulation: Changes are detected by the circumventricular organs (SFO and OVLT), which then go on to trigger thirst and ADH secretion.
**The areas in which these mechanisms of regulation intersect exist because the sympathetic N.S. and RAAS trigger both thirst and ADH release as well (highlighted portions on the chart).
143
Imagine you are asked to look down the barrel of a microscope at section of kidney tissue; at the top of your viewer is the upper edge of the renal cortex and at the bottom of your viewer is a portion of the renal pelvis. You make a few key anatomical observations: practically all the glomeruli in this kidney are localized in the superficial cortex, the renal medulla is very short compared to the cortex, and practically all the loops of henle seem to only extend through half the length of the renal medulla. Based on these observations, what predictions could you make regarding the climate that this animal inhabits?
This animal's kidneys exhibit mostly cortical nephrons, meaning that water conservation is probably not as important. We can then extrapolate that the animal lives in a wet habitat where water is plentiful and need to concentrate urine is not a priority.
144
What are the 5 functions of Angiotensin II
1. Stimulates Aldosterone release- inc. sodium reabsorption in distal tubule/collecting duct
2. Stimulates Na+/H+ exchanger in prox. tubule
3. causes vasoconstriction of afferent arterioles-renal and systemic blood vessels (dec. flow to glomerulus)
4. Enhances tubuloglomerular feedback system — (macula densa cells respond to tubular fluid flow quicker—> vasoconstriction of Afferent arteriole—>dec. GFR)
5. Stimulates thirst- it acts on the hypothalamus to stimulate thirst and stimulates release of ADH as well; thirst leads to water consumption, causing an increase in water reabsorption in distal tubule and collecting ducts
145
What's the main overarching goal of all 5 functions of Angiotensin II
recovering plasma volume
146
If I were to tell you that the clearance rate of substance X is equal to glomerular filtration rate, then how is substance X handled by the kidneys?
It is “freely” filtered- meaning it is not attached to any plasma proteins, etc.
Cannot have undergone any reabsorption
Cannot have undergone any secretion
Has to have a stable concentration in the blood
147
How is creatinine handled differently by the kidneys compared to substance X?
There is a small bit of secretion of creatinine
148
Compare and contrast the use of plasma creatinine vs. BUN levels in assessing renal function.
When GFR declines Plasma creatinine increases proportionately (inversely proportionate)
Is useful for monitoring the progress of chronic rather than acute renal disease
because it takes 7-10 days for the plasma Creatinine to stabilize
when GFR declines
When GFR declines, BUN also increases - BUT, BUN also increases if there is an increase in water reabsorption (whereas creatinine only increases if BUN goes down- doesn't get reabsorbed like BUN does)
BUN rises in states of dehydration and acute
and chronic renal failure (also varies as a result of altered protein intake and protein catabolism )
149
A patient visits her healthcare provider complaining of urinary tract infection symptoms (burning upon urination, increased urinary frequency). This patient also has uncontrolled diabetes. What urinalysis findings would you expect for this patient?
- cloudy urine, odorous urine;
- alkaline level is high
- glucose in the urine
- ketones in urine
- Bacteria via urine sed. analysis
150
What exactly are kidney stone? What are the stones usually made of? What factors increase the risk for stone formation?
“Renal calculi”
Develop within the kidneys, travel into renal pelvisàinto ureters where they can get lodged and cause obstructions
Kidney stones are solid masses of collection of tiny crystals; these clump together to form a stone; 1 or more present at same time: calcium, oxalate, uric acid
Men have higher risk b/c have higher GFR and filtration rate of constituents, longer tract
Causes
Hypercalciuria;
Decreased levels of urinary Magensium
A low fluid intake
151
What symptoms are associated with all forms of prostatic enlargement?
an be caused by acute inflammation, benign prostatic hyperplasia, or prostate cancer; have the same symptoms, including:
Urinary frequency
Urinary urgency
Urinary hesitancy
Incomplete bladder emptying (straining)
152
What is the most common cause of prostatic enlargement?
Benign Prostatic Hyperplasia
153
What is PSA testing and what can it tell you?
Detection of prostate cancer; blood test
Prostate Specific Antigen- protein found on prostate cells; concentration of PCA is correlated to total prostate mass; inc in mass causes inc in PCA
Cancer- PCA will be higher than enlargement from BPH
154
renal handling of insulin
no reabsorption, no secretion, does not impact GFR: but is not a stable plasma concentration- have to be attached to a drip of insulin
155
What is the difference between acute prerenal failure and ischemic acute tubular necrosis?
Pre-renal: if you don’t re-perfuse kidneys will become ischemic acute tubular necrosis
Ischemic Acute Tubular necrosis- BF was not returnedprogressed into intrarenal failure
156
Acute Renal Failure
Defined as a precipitous and significant (>50%) decrease in glomerular filtration rate (GFR) over a period of hours to days, with an accompanying accumulation of nitrogenous wastes in the body.
almost always completely reversible
3 main mechanisms: pre renal failure, infrarenal failure, post obstructive renal failure
157
Prerenal failure:
GFR is depressed by compromised renal perfusion.
158
Intrinsic renal (Intrarenal) failure
includes diseases of the glomerulus or tubule,
which are associated with release of renal afferent vasoconstrictors.
intrarenal disorders: obstructive disorders
obstruction in the flow of urine from the kidneys to the bladder and/or from bladder to external environment
when an obstruction occurs ABOVE the level of the bladder, it’s called an upper tract obstruction (below the bladder is called a lower tract obstruction)
159
Main causes of LVH
anything that increases afterload
- aortic stenosis (or any type of obstruction preventing blood flow)
- hypertension
160
What is Left Ventricular Hypertrophy (LVH)?
LVH is when you have an enlargement of the left ventricle - this is the main ventricle in pumping blood throughout systemic circulation (very high pressure system). LVH is the body’s way of compensating for an increase in pressure. Hypertension leads to left ventricular hypertrophy as a result of increased workload imposed on the heart.
161
Factors that Determine Myocardial O2 Demand:
```
Heart rate
Contractility
Overall workload (preload/afterload)
Wall tension
remember that wall tension is a FORCE
wall tension is the amount of force necessary to generate a given left ventricular pressure at a very particular left ventricular radius:
LV SP X LV radius
LV wall thickness
```
162
heart rate and diastolic time are ____ correlated
inversely
increase in heart rate will decrease diastolic perfusion time
163
Right coronary artery perfuses:
the anterior of the right side of the heart (following the atrioventricular groove)
the inferior wall of the right side of the heart
posterior and inferior/lateral walls of the left ventricle
164
***Left anterior descending branch of the left coronary artery perfuses:
anterior surface of the heart
intraventricular septum (purkinje fibers and bundles of His)
165
Left circumflex branch of the left artery perfuses:
lateral and posterior wall of the left ventricle
166
Question: Mr. C is a 69 y/o male brought into the ED for chest pain consistent with MI. Due to positive cardiac enzymes, he is brought into the cath lab. It is found that he has a proximal left anterior descending artery obstruction. Which of the following correctly describes the area of myocardial cell death?
Intraventricular septum and anterior surface of the heart
167
chronic ischemic heart disease:
silent ischemia (most common)
stable angina (a predictable amount of chest pain that is usually caused by physical activity)
variant angina
168
acute coronary syndromes:
MI (STEMI, NSTEMI)
unstable angina (looks like MI but no death of cardiac tissue) “dynamic flow changes”
169
ST segment depression is most commonly associated with
“demand ischemia” (upon exertion, e.g. exercise testing, stress test)
170
ST segment elevation (anywhere above 1 mm) is most commonly associated with
“supply ischemia” (upon occlusion) - this indicates a transmural effect (i.e. the wall of the heart is undergoing ischemia and possible necrosis)
171
ECG MI signs
ST elevation
prominent Q wave
T wave inversion
172
What ECG changes are consistent with acute MI? Are the different ECG changes thought to correlate to location or severity of the MI?
Acute MI: can be STEMI or NSTEMI
ST segment elevation suggests a more serious MI and a prominent Q wave
Triponin is test of choice
173
Right Coronary Artery (RCA) Obstruction:
- Moderate to large inferior (posterior, lateral, right ventricular) - if proximal RCA is occluded
- Small Inferior (if distal RCA is occluded)
174
Left Anterior Descending (LAD) Artery Obstruction:
- Proximal LAD (aka “the widow maker”): High mortality, occlusion is located proximal to the first septal perforator, compromised perfusion to his-purkinje conduction tissue
- Mid LAD
- Distal LAD (less common)
175
Left Circumflex Artery Obstruction
- Moderate to large inferior (posterior, lateral, right ventricular)
- Small inferior
176
What is the most common cause of acute MI?
Blood clot that arises from rupture of atherosclerotic plaque and causes either partial or complete occlusion
177
Why are chronic large vascular plaques not usually the cause of acute MI?
(1) Because they aren’t getting as much force as the smaller plaque (blood will divert towards an area of lesser occlusion)
AND
(2) larger plaque will have a higher protein-to-fat ratio (more protein) making it more stable and less likely to rupture
178
Why does the infracted myocardium heal through fibrosis rather than by regeneration?
Myocardium cannot regenerate - instead, it goes through Cardiac remodeling - necrosis triggers inflammatory response which causes fibrosis
179
Why, would you guess, is it dangerous to give steroid or anti-inflammatory drugs to individuals in the weeks following an acute MI?
- NSAIDs prevent inflammatory response from occurring and myocardium from healing itself
- Trying to prevent ventricular rupture here***
180
“Collateral circulation” is angiogenesis:
formation of new vessels due to some sort of partial or complete obstruction that’s causing decreased flow to one part of the myocardium so increased formation of new vessels will occur to compensate/try to increase supply to that area
This will have a POSITIVE effect on the outcome of an acute MI - although the tissue might be ischemic, it won’t be nearly as ischemic as it would if it didn’t have the collateral circulation
181
Why do post MI patients have an increased risk for cardiac arrhythmias?
Because anytime you have cardiac remodeling, it will affect the pathways of electrical conduction - these trajectories will be changed and increase the risk for cardiac arrhythmias
182
How do digital rectal exam findings differ in patients with prostate cancer vs. those with benign prostatic enlargement?
Cancer:
- nodular
BPH:
- symmetrical enlargement
"boggy" or spongy indicates inflammation
183
PAH estimates what?
Renal blood flow
184
Cystatin C is
produced by all nucleated cells
rate of production is thought to be constant, unaffected by gender, age, muscle mass
185
Renal handling of creatinine
inverse relationship
a long term decline in GFR over weeks/months is reflected in the plasma creatinine concentration
186
Normal creatinine is
0.7-1.2 mg/dl
187
it takes ___ days for plasma creatinine to stabilize when GFR declines
7-10 days
188
as osmolarity goes up, specific gravity goes ___
up
189
uncontrolled diabetics will have ___ and ___ in urine
glucose, ketones
190
clinically, what is the generally accepted measure of functional renal (nephron) mass and therefore renal function
GFR
191
Post obstructive renal failure
initially causes an increase in tubule pressure, decreasing filtration driving force
Obstruction of urinary flow out, building up of pressure causes DECREASED GFR
192
What is the most common cause of Post obstructive renal failure? What sex/age group would predominate?
Urinary obstruction
older males
193
LVH increases the risk of what 4 things?
1. Ventricular arrhthmias
2. Sudden cardiac death
3. Death from MI
4. Chronic heart failure
194
factors that determine myocardial O2 supply (5)
1. Diastolic perfusion pressure and diastolic time
2. Coronary vascular resistance
3. O2 carrying capacity
4. O2 extraction
5. Ventricular wall compression
195
Endothelium senses change in metabolites and releases ____ to cause dilation, or ___ to cause constriction
nitric oxide = dilation
endothelien = constriction
196
What is the intrinsic mechanism of controlling coronary vascular resistance?
endothelium processes of dilation or constriction
197
What is the main difference between chronic ischemic heart disease and acute coronary syndromes?
Chronic ischemic heart disease is a consequence of ATHEROSCLEROSIS of the coronary arteries and develops when BLOOD FLOW IS INADEQUATE (over time)
in acute coronary syndromes, it's a SUDDEN onset caused by RUPTURE OF A PLAQUE (will always be symptoms)
198
Is cardiac ischemia always symptomatic?
no
199
3 main categories of cardiac ischemic pain
1. A diffuse visceral component (don't feel well but can't pinpoint what it is - "impending sense of doom")
2. Better defined somatic component confirming to distribution of dermatomes (referred pain)
3. Interpretive component modulated by psychological factors (shows how every patient is different and can experience the same event differently)
200
how is referred pain very different for men and women?
only 30% of women will feel "classic" hear pain - will more likely by in GI or back of jaw
their pain may be more sharp/stabbing than male counterparts
201
What are the principle features (s/s) in the clinical definition of unstable angina?
unstable angina is either new-onset chest pain OR chest pain that occurs AT REST (not relieved by nitroglycerin or resting)
no necrosis of myocardial tissue, but there is ischemia
202
What is the clinical definition of MI?
Evidence of myocardial necrosis consistent with ischemia
203
What are the classic symptoms of MI
- intense, opposrive chest pressure with impending sense of doom and radiation of paint to left arm
- also common is: pale skin, tachycardia, elevated BP
- other symptoms related to fear response: n/v, dyspnea
204
signs of MI
- detection of biomarkers (esp. Troponin)
| - ECG: ST elevation, prominent Q wave, T wave inversion
205
MIs can be classified in what 3 ways?
1. By size (microscopic, moderate, large...or 10-20%, >30% of LV myocardium respectively)
2. ECG changes
3. By location (anterior, posterior, lateral, etc.)
206
What ECG changes are consistent with acute MI?
STEMI or NSTEMI
ST segment elevation and more prominent Q wave suggest for serious MI
Troponin is test of choice
207
What is the rationale for using diuretics to help treat CHF?
they help to limit the fluid retention
208
What is the rationale for using Digoxin to help treat CHF?
specifically tends to increase the contractility of the heart - this is given in the much later stages of heart failure, to elderly, in order to maintain minimal heart function if the heart failure has progressed very far
209
What is the rationale for using Beta Blockers to help treat CHF?
will decrease heart rate with the goal of reducing the oxygen demand on the heart (reduce the heart rate, you reduce the oxygen demand on the heart) — trying to preserve cardiac function
210
What is the rationale for using Aldosterone antagonists to help treat CHF?
specifically aimed at limiting sodium and water retention caused by aldosterone
211
What is the rationale for using Angiotensin Receptor Blockers to help treat CHF?
similar to ACE inhibitors, but are specifically blocking the receptors to angiotensin
212
What is the rationale for using ACE inhibitors to help treat CHF?
reduce the production of Angiotensin II, which reduces volume overload and reduces vasoconstriction and will help limit the activation of the Renin-Angiotensin system
213
What drugs are commonly used to treat CHF?
- Ace Inhibitors
- Angiotensin Receptor Blockers
- Aldosterone antagonists
- Beta blockers
- Digoxin
- Diuretics
214
How are HF patients clinically categorized with respect to treatment recommendations? What 4 categories?
At Risk for Heart Failure:
STAGE A: High risk for developing HF
STAGE B: Asymptomatic LV dysfunction
Heart Failure:
STAGE C: Past or current symptoms of HF
STAGE D: End-stage HF
215
What are the key pathological features and progression of Chronic Heart Failure? Explain how the body's compensation mechanisms for a failing heart only worsen the condition
It starts with a moderate decrease in cardiac output
Body compensates by increasing HR, contractility --> increasing the workload of the heart to try and recover CO
This sets the already damaged heart up for more ischemia/damage - causes an even further decline in CO, which is responded to by more compensation (further increase in workload)
216
What does reabsorption do to the clearance rate?
Any amount of reabsorption decreases the clearance rate
217
What does secretion do to the clearance rate?
speeds up
218
people with reduced renal function will need ___ doses of drugs
lower
219
Plasma clearance rate (ml/min) can be calculated by:
= [Urine] for substance X Urine flow rate (quantity/ml urine)
__________________________________
[plasma] of substance
(quantity/ml plasma)
220
if you have long-term decline in GFR, you will see an ____ in plasma creatinine
elevation
221
What is plasma creatinine useful for measuring?
Is useful for monitoring the progress of chronic rather than acute renal disease
because it takes 7-10 days for the plasma Creatinine to stabilize
when GFR declines
222
2 things that determine urea concentration:
- GFR (if it goes down, BUN goes up)
| - increased water reabsorption (BUN also goes up)
223
if osmolarity goes up, specific gravity goes
up
224
higher concentration of uric acid can increase
crystal formation
225
casts
strips of cells that are actually the interior epithelium of the renal tubule - can be seen in sediment analysis - highly suggestive of acute tubular necrosis/injury
226
the most common source of reduced renal function is
aging
227
most important consequence of aging on renal function is
decreased rate of excretion
228
most common obstructive intrarenal disorder
kidney stones (also called renal calculi)
majority of kidney stones have calcium
229
where do we see elevated calcium levels that could increase urinary calcium (aka affect kidney stone formation)?
Hypercalciuria: osteoporosis, conditions where people are on corticosteroids, overconsumption of calcium
Decreased levels of urinary Magnesium (Magnesium interferes with stone formation, so if it’s low, the likelihood of stone formation is higher)
A low fluid intake
230
Polycystic Kidney Disease:
A genetic disorder characterized by the growth of numerous fluid-filled cysts in the kidneys.
PKD cysts can slowly replace much of the mass of the kidneys, reducing kidney function and leading to kidney failure.
231
What is the most common (inherited) form of Polycystic Kidney Disease?
Autosomal dominant PKD: most common (90%), Symptoms usually develop between the ages of 30 and 40
232
Autosomal recessive PKD:
rare, Symptoms of autosomal recessive PKD begin in
| the earliest months of life, even in the womb
233
Acquired cystic kidney disease (ACKD):
develops in association with long-term kidney problems, especially in patients who have kidney failure and who have been on dialysis for a long time
234
most common symptoms of PKD
pain in the back and the sides (between the ribs and hips), and headaches.
The dull pain can be temporary or persistent, mild or severe
235
Almost all UTIs are __ in origin
ascending
means that bacteria is coming from external genitalia and moving back up the tract
236
metabolic changes like ___ increase risk of UTIs, as do use of what meds?
hyperglycemia
broad-spectrum antibiotics (b/c they kill normal bacteria in the lower tract
237
What is the definition of Hydronephrosis? what can it lead to?
a dilation of the renal pelvis and calyces.
Renovascular Hypertension (due to reduced renal blood flow)
238
most common organism to cause UTIs is
E.coli — from fecal matter
239
What gender is UTI more common in?
much more common in women than men b/c women have very short lower urinary tract (less space for bacteria to travel than men)
240
Postobstructive renal failure initially causes
an increase in tubular pressure, decreasing the filtration driving force.
241
anything that reduces renal blood flow makes people susceptible to pre renal failure, such as:
hypovolemia (burn, lost albumin and fluid)
hemmorage
dehydration
any form of shock (if BP goes down, you’re not perfusing kidneys)
heart failure
242
With treatment each type of renal failure progresses through three distinct phases:
1. Oliguric phase (decreased urine output)
2. Diuretic phase (increased urine output)
3. Recovery phase (GFR normalizes)
243
Renal insufficiency
decline of about 15% of normal GFR and elevated
| serum creatinine and urea
244
Renal failure
significant loss in renal function (when less than 10% left –
end-stage renal failure)
245
Azotemia
increased serum urea levels and frequently increased creatinine levels
– renal insufficiency and failure cause Azotemia
elevated urea and creatinine
246
uremia
a syndrome of renal failure that includes urine in the blood (increase in blood urea) and creatinine levels accompanied by fatigue, anorexia, nausea, vomiting, pruritis, and neurological changes
247
Hyperkalemia in chronic renal failure can lead to
cardiac arrest
248
low erythropoietin in chronic renal failure causes
anemia
249
acidosis in chronic renal failure causes
skeletal buffering and osteodystrophies (demineralization of the bone)
250
loss of phosphate and vitamin D in chronic renal failure causes
persistent hypocalcemia and hyperparathyroidism (breaks down bone to liberate calcium)
251
hemodialysis
uses principle of diffusion and filtration in order to filter your blood in lieu of your kidneys doing it - blood is surrounded by dialysis fluid to encourage movement of things like potassium and phosphate OUT of the blood and the movement of bicarbonate and calcium INTO the blood - when blood moves out of dialysis machine, the composition is normal
can take 3-4 hours at sitting
up to 3 days or more a week
252
kidneys are filtering organs AND
endocrine and metabolic organs
253
one of the most important hormones that the kidney produces is:
EPO (erythropoietin) - acts on bone marrow and stimulates RBC production
254
If capillary blood pressure goes up, GFR goes
up
255
If Plasma Colloid Osmotic Pressure or Bowman’s Capsule Hydrostatic Pressure goes up, GFR goes
down
256
when our BP increase, glomerular capillary BP increases, which increases
net filtration pressure —> causes increase in GFR
257
If Arterial BP drops, auto regulation will cause efferent arteriole to
VASODILATE
258
rise in BP, efferent arteriole will
constrict
259
BP rises – causes temporary rise in GFR and increased rate of fluid flow through distal tubule – macular densa cells stimulate granulosa cells to release a
vasoconstrictor
260
sympathetic nerves release epinephrine and norepinephrine on the smooth muscle on the arteriole which bind to alpha adrenergic receptors and cause
constriction - -will cause decrease in GFR
261
example of extrinsic control of GFR (hemorrhage)
decrease in blood volume that causes drop in BP, activates SNS, decreased GFR and urine production - you’re conserving plasma and BP
262
of all of the things that we reabsorb, we dedicate the MOST energy to reabsorbing
sodium
263
What are the main elements we reabsorb?
sodium
potassium
phosphate
glucose
264
Reabsorption of Na+ in the proximal tubule
plays a crucial role in the reabsorption of
| glucose, amino acids, water, and urea
265
Reabsorption of Na+ in the ascending limb of the loop of henle
plays an important role in the kidneys ability to
| concentrate urine and conserve water
266
Reabsorption of Na+ in the distal tubule and the collecting duct
under hormonal control and plays a role in
| regulating ECF volume and blood pressure
267
the general pattern for reabsorption anywhere in the renal tubule (2 parts):
1. sodium has to cross the luminal membrane either through a passive channel OR through some sort of co-transporter (sodium enters the cell, moves down concentration gradient, and frees up energy to move something in or out)
2. sodium crosses the basolateral membrane via the Na/K ATP pumps — tons of these pumps are in the lateral membrane — all pumping sodium across and into the blood
268
what’s the limiting factor that determines saturation point for facilitated diffusion?
the number of available carrier proteins
269
the descending loop of Henle is the ONLY part of the nephron where ___ is not reabsorbed
sodium
270
the ascending loop of Henle is the ONLY part of the nephron where ___ is not reabsorbed
water
271
throughout the tubule, water reabsorption is always
secondary to sodium reabsorption
passive and always occurs downhill through osmotic gradient - goes from dilute area to more concentrated area
272
important substances to be secreted during tubular secretion (3)
hydrogen ions — when we are secreting hydrogen ions, we are getting rid of excess acid and adjusting overall blood pH
potassium — we are ridding ourselves of additional potassium ions
organic cations and anions — organic molecules that are positively and negatively charged - include drugs, environmental pollutants, additives (can also be endogenous like hormones)
273
Potassium undergoes both
reabsorption and secretion
274
In the proximal tubule, potassium is reabsorbed via
passive diffusion is much the same way as Cl- and urea
| following water reabsorption
275
Potassium reabsorption is ___, while potassium secretion is ____ regulated
unregulated
| hormonally
happens in collecting duct and distal tubule
276
aldosterone is a mineralcorticoid because it
brings about sodium retention and potassium loss in the distal tubule and collecting duct
— it enhances sodium reabsorption and stimulates potassium secretion
277
potassium secretion occurs in ____ and ____ and is happening simultaneously with ____
occurs in distal tubule and collecting duct
is happening simultaneously with sodium reabsorption
278
if Organic Anion and Cations are bound to albumin when they enter the glomerulus, they
won't be filtered
279
reabsorption ____ the rate of clearance/excretion
slows down
280
secretion ____ the rate of clearance/elimination
speeds up
281
if blood osmolarity increases, it causes
cell shrinkage
282
if blood osmolarity decreases, it causes
cell swelling
283
Two elements that control total-body water and therefore osmolarity
1) the kidneys control of water excretion
| 2) the thirst mechanism that controls oral intake of water
284
In healthy individuals, plasma osmolarity is about
290 mOsm
285
Increases by as little as 1% in plasma osmolarity can produce a large increase in
plasma [ADH]
286
Increased LDLs lead to
increased oxidized LDLs which damage endothelium and lead to atherosclerosis
287
What is a fatty streak?
A thin accumulation of lipid, in the form of foam cells, in the intima of medium to large sized arteries.
Normal to find these in children even as young as 1 year old, increase in number until age 20 and then plateaus.
It is a normal, intermediate healing stage as a result of acute endothelial injury (analogous to a scab).
It can also lead to an atherosclerotic plaque if the source of the injury is persistent.
288
Foam cells
lipid-engorged macrophages
289
Intima
innermost layer of artery wall
290
What are the physical features of a plaque?
Fibrous cap, has collagen, foam cells and necrotic core
291
What factors influence the likelihood that an atherosclerotic plaque will rupture?
Stress on the cap
Overall weakness of the cap
Therefore, small and new plaques are most likely to rupture. These plaques are more likely to be asymptomatic.
292
What are the three conditions that promote thrombosis anywhere in the cardiovascular system?
Virchow’s Triad:
1. Endothelial injury
(Chronic – atherosclerosis
Acute – damage that exposes the lamina (catheter procedure))
2. Sluggish blood flow
(clotting - Valve abnormalities, bed rest, fibrillation of the heart, travel)
3. Increased coagulation
(Inherited coagulopathy, Temporary hypercoagulation state – pregnancy, hormones)
293
What is an embolus? What is the most common cause of an embolus?
Embolus: anything foreign in the blood stream that is traveling that shouldn’t be there
Most common cause is a plaque that broke off.
294
Embolus in venous system (DVT):
embolus travels up into the right side of the heart, lodges in the lungs causing a pulmonary embolus
295
Embolus in arterial system:
commonly formed in the left side of the heart (a-fib or valve problems), travels and limits blood flow to tissue, could cause a stroke or infarction of organ tissues
296
What is the difference between primary and secondary hypertension?
Primary (aka essential) HTN: not a clear reason as to what caused it, 90% of cases
Secondary HTN: secondary complication of a primary disease (renal problems, endocrine problems, etc.)
297
What are the major risk factors for primary hypertension?
Obesity, smoking, age, gender, race, potassium deficiency, excess sodium
298
What are the three major hypothesized categories of genetically linked physiological alterations that may lead to the development of primary hypertension?
1. Inadequate sodium excretion (salt sensitivity)
2. Vascular wall thickness
3. Increased vascular reactivity
299
What two ethnic/racial groups seem to be similar in their increased risk for primary hypertension?
People of African decent (Sub-Saharan except for South Africa)
Japanese decent
300
What are “White Coat Hypertension” and “Masked Hypertension”? By what method can you screen someone for these conditions?
White Coat HTN: false positive, people who are more likely to have higher BP in clinical settings, these people have higher anxiety levels in general
Masked HTN: false negative, some people are at lower stress in clinical setting than in the rest of their life, so they are spending most of their day hypertensive but not when in the clinical setting
Screen somebody for these conditions with a 24-hour ambulatory blood pressure measurement – allows you to get an average blood pressure
