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Conj 403 > Midterm 2 - Amanda > Flashcards

Midterm 2 - Amanda Flashcards

1
Q

Respiration changes in pH

A

Increasing CO2 is called respiratory acidosis
Decreasing CO2 is called respiratory alkalosis. Hyperventilation

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2
Q

Metabolic Changes in pH

A

Metabolic acidosis is build up of lactic acid when compensating for respiratory alkalosis.
Metabolic alkalosis: Side effect of certain drugs but does not arise physiologically.

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3
Q

Large Passageways of Respiration

A

nasal passages contains conchae and sinuses which moisten, warm and clean the air flowing through. Then pharynx containing MALT. Next, larynx. Next, trachea which leads to the primary bronchus then secondary etc… all the way to ten branchings.

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4
Q

Bronchioles

A

Airways without cartilage. Terminal bronchioles branch to respiratory bronchioles which doesn’t have a complete epithelium. These leads to alveolar ducts with no epithelium.

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5
Q

Pulmonary Artery

A

The pulmonary artery follows the branching of the pulmonary bronchi and is visible in a pulmonary angiogram.

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6
Q

Airway Epithelium

A

ciliated epithelium. Goblet cells and submucosa glands excrete mucus and fluids. Basal cells regenerate the other cells.

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7
Q

Chronic Bronchitis

A

usually arises in COPD patients and is associated with cigarette smoking. Involves the continual inflammation of the airways. Hypertrophy of submucosa glands, lose ciliated cells and basal cells start dividing uncontrollably.

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8
Q

Regulation of Airway Smooth Muscle

A
  1. Parasympathetic: contraction of smooth muscle
  2. Sympathetic: Dilation of smooth muscle
  3. Inflammatory paracrine: constrict airways. Examples are histamine, phospholipase A2 and leukotrienes.
  4. Carbon Dioxide: increase leads to smooth muscle dilation.
  5. Neural Reflexes: Occurs through the stimulation of afferent neurons by irritants in the airway. Causes constriction of smooth muscle.
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9
Q

Regulation of Submucosa Glands

A
  1. Parasympathetic: Stimulates secretion
  2. Inflammatory paracrine: stimulate secretion
  3. Neural Reflexes: Irritant stimulates sensory afferents activating the parasympathetic neurons causing secretion.
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10
Q

Ion/Fluid Transport in Epithelium of Airways

A

Regulated step is the net movement of chloride ions from the interstitial space to the lumen. Chloride channel is opened through cAMP phosphorylation.

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11
Q

Alveolar Cells

A

type I, type II, endothelial, fibroblasts, macrophages, neutrophils

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12
Q

Atelectasis - definition and causes

A

Collapse of a lung in which a gap opens in the pleural space.

1- Obstructive atelectasis: caused by a clogged bronchus. May be due to a tumor, mucus or a pea.

2- Absorptive atelectasis: occurs when patient is on oxygen therapy

3- Pneumothorax: air or gas in the intrapleural space. Causes may be a wound to the chest wall, or serious infections like TB.

4- Spontaneous pneumothorax: no obvious cause, the lung simply pulls away from the chest wall.

5- Surfactant problem: less surfactant causes more tension in the alveolar walls which makes the lung easier to collapse.

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13
Q

IRDS

A

infant respiratory distress syndrome

develops in premature infants because surfactant has not developed yet.

Symptoms include tachypnea (fast breathing) and cyanosis (refers to the blue color of deoxygenated hemoglobin especially under fingernails and in the lips)

Restrictive lung disease.

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14
Q

Surfactant

A

made of phospholipid and four amphipathic proteins. Responsible for changing surface tension based on surface area. Smaller surface areas have smaller surface tensions.

Law of Laplace and surfactant: if alveoli of different sizes didn’t have similar surface tension they would have different pressures and smaller alveoli would collapse. Problem in IRDS

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15
Q

Muscles used in ventilation

A

quiet breathing: diaphragm, external intercostals for inhalation. exhalation is passive

exercising: Internal intercostals and abdominal muscles aid in active exhalation. Neck muscles also aid in inhalation.

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16
Q

Total lung capacity

A

maximum amount of gas in lungs after maximum inhalation

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17
Q

Forced Vital capacity

A

maximum amount of gas you can exhale

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18
Q

FEV1

A

Maximum amount you can exhale in the first second

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19
Q

Residual volume

A

gas left in lung following maximum exhalation

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20
Q

Functional residual capacity

A

amount of gas in lungs following a normal exhalation. Changes in asthma and COPD

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21
Q

Alveolar Ventilation

A

defined as the amount of new air entering the alveoli per minute. = f * (Vtv - Vds) where f is the frequency of ventilation

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22
Q

Tidal volume

A

the amount being inhaled and exhaled at any given time

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23
Q

Alveolar gas

A

upon inhalation it is the first gas that goes into the alveoli but is not fresh because it was the gas left in the airways from the last exhalation.

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24
Q

anatomical dead space

A

volume of gas left in the airway and is approximately equal (in mL) to the persons weight in pounds

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25
Q

ARDS - causes, characteristics and pathology

A

Acute respiratory distress syndrome

epithelial inflammation

Causes: serious infection, sepsis

Characteristics: dyspnea signals the onset. hypoxemia which is inadequate oxygenation of the blood. hypercapnia which is not blowing carbon dioxide off fast enough. Protein rich infiltrates accumulate in the alveoli.

Pathology: Neutrophils join macrophages in the alveoli causing hyper-inflammation

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26
Q

Asthma - epidemiology

A

prevelance is greater than 20 years ago. Higher prevalence in boys in a younger age but girls in older ages.

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27
Q

Asthma - general

A

Obstructive disease with inflammation that leads to airway hyper-responsiveness. Is reversible to some extent.

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28
Q

Atopic Asthma

A

genetic predisposition and environmental factors TH2 cells dominate instead of TH1 which would be a normal response. TH2 cells release cytokines and IgE resulting in high levels of inflammation.

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29
Q

Atopic Asthma sequence

A

Within the first hour: mast cells release inflammatory paracrines such as histamine and leukotrienes causing smooth muscle contraction, edema and mucus secretion.

After 4-6 hours: cytokines with infiltration of cells. Airways become hyper-responsive.

Weeks to months: airway remodeling. Walls and basement membranes thicken and there is goblet cell hyperplasia (have more goblet cells)

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30
Q

Non-atopic asthma

A

stimulus (cold air, cigarette smoke, exercise) stimulates afferent neurons in the airways which can begin a reflex that either acts locally or via the CNS to cause smooth muscle contraction and submucosal gland contraction

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31
Q

Asthma - treatments

A

remove or reduce exposure to the allergen

Inhaled short-acting Beta-2 agonist: first choice.

Inhaled corticosteroid: fluticasone. suppresses inflammation to prevent asthma Inhaled

long-acting beta-2 agonist: salmeterol. always given with a inhaled corticosteroid. Oral drugs are contraindicated.

Leukotriene receptor antagonist or a blocker of lipooxygenase.

Anti-IgE monoclonal antibody

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32
Q

Chronic Bronchitis and Emphysema

A

COPD or chronic obstructive pulmonary disease. Common in smokers.
High functional residual capacity due to the difficulties with exhalation.

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33
Q

Airway Damage in COPD

A
  1. epithelial damage including loss of cilia, degenerative epithelial cells and abnormal repair.
  2. Submucosal glands hypertrophy and mucus production is over-stimulated
  3. Small airways thin and lose support which, during exhalation, causes the pressure surrounding the airways to be greater than atmospheric, making it hard to exhale.
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34
Q

Alveolar Damage in COPD

A
  1. destruction of alveolar walls leads to abnormally large air spaces within the lung called bullae.
  2. Neutrophils release proteases, such as neutrophil elastase that break down elastic connective tissue. 3. Phagocytes also release proteases and oxygen radicals that damage surrounding tissue.
  3. Antiproteases, which are normally released by macrophages as protection, are genetically deficient.
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35
Q

Mismatching of Ventilation and Perfusion

A

Unequal distribution of blood flow to the lungs due to destruction of capillaries. Lowers the partial pressure of oxygen leaving the lungs and may result in hypoxemia (low oxygen in blood).

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36
Q

Treatment in COPD

A
  1. First is smoking cessation
  2. Inhaled short-acting beta-2 agonist. Albuterol. Rescue inhaler.
  3. Inhaled short-acting anti-cholinergic. Ipratropium.
  4. Inhaled long-acting beta-2 agonist. Salmeterol. Improve FEV1 but do not affect course of disorder.
  5. Inhaled long-acting anti-cholinergic. Tiotropium. Improve FEV1 but do not affect course of disorder.
  6. Inhaled corticosteroid. Fluticasone. Not used alone but may be combined with inhaled long-acting beta-2 agonist to improve FEV1 but does not affect course of disorder.
  7. Oxygen therapy. Only used if PaO2 falls below 55 mm Hg.
  8. Lung Reduction Surgery. Remove the worst part of the lung and allow the rest of the lung to regenerate the area.
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37
Q

Characteristics of Restrictive Lung Disease

A

Defined by having a normal FEV1/FVC ration. However, have an abnormally low FVC meaning inhalation is very difficult.

Low compliance of lungs (in contrast to asthma and emphysema).

Common symptom is dyspnea (difficulty breathing).

Finally, there is impaired diffusion of oxygen between the alveoli and the capillaries.

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38
Q

Normal Lung healing

A

Type 1 cells are most commonly damaged and if the connective tissue matrix remains intact type 2 cells will divide and develop into type 1 cells. If the connective tissue matrix is damaged it sometimes can be repaired but beyond a certain amount of damage nonfunctional scar tissue forms.

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39
Q

Occupational Restrictive Disorder

A

Examples are asbestosis and silicosis.

Macrophages release growth factors which drives processes creating fibrosis of the lungs.

Abnormalities in the replenishment of type I cells and impaired mucosal defense mechanisms are present.

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40
Q

Idiopathic Pulmonary Fibrosis

A

Unknown cause. Common in people over 50. Extensive fibrosis and low survival rates after a few years.

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41
Q

Sarcoidosis

A

inflammatory disorder of unknown cause. Characterized by accumulation of macrophages which is called granulomas.

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42
Q

Bronchiectasis

A

chronic, abnormal dilation of the bronchi. Presents with persistent productive cough and recurrent airway infections

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43
Q

Cystic Fibrosis

A

Genetic disorder involving defective chloride channels. Mucus clogs the lungs which promotes serious lung infections.

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44
Q

IRDS and Laplace

A

infant respiratory distress syndrome. In normal alveoli with surfactant, surface tension in small alveoli is reduced more compared to the larger alveoli. Without surfactant the surface tension is the same in both large and small alveoli. According to the Law of Laplace, if tension is the same pressure decreases with increasing radius. Because smaller alveoli have higher pressure, gas will flow from small alveoli to larger alveoli. Blood leaving the lungs contains less oxygen than normal because of collapsed small alveoli, causing cyanosis.

Also, compliance is less with low levels of surfactant causing inhalation to be difficult.

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45
Q

Pneumonia

A

general term that refers to infection of the lung with subsequent solidification of the tissue. Alveoli fill with edema followed by a rapid accumulation of macrophages and neutrophils. Sometimes damage may cause thickening of the airway causing bronchiectasis

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46
Q

Tuberculosis

A

Activated macrophages accumulate to form a granuloma. Usually leads to significant necrosis and fibrosis. Secondary tuberculosis develops when the bacteria which were contained in a granuloma emerge

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47
Q

Carcinoma of the lung

A

most common cause of death from cancer in the US. Caused by smoking 90% of the time.

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48
Q

Common partial pressures

A

PO2 inhaled = 160 mm Hg. PCO2 inhaled = 0.3

PAO2 (alveolar) = 105 mm Hg. PACO2 = 40 mm Hg.

PvO2 (entering right atria) = 40 mm Hg. PvCO2 = 46 mm Hg but both these values are variable and depend on exercise

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49
Q

Oxygen in solution

A

To determine you multiply the partial pressure by the solubility at body temperature which is 0.03 mL O2 / L -mm Hg. Normal PaO2 is 100 mm Hg so oxygen in solution would be 3 mL O2/L.

However, when measured O2 in blood is about 200 mL O2/L. Therefore can conclude that hemoglobin accounts for nearly all the oxygen in the blood.

50
Q

Oxygen bound to hemoglobin

A

Determine percent saturation of hemoglobin with the oxygen dissociation curve for hemoglobin.

To determine the amount of oxygen hemoglobin holds use the constant of 1.39 mL O2/gram Hb.

Can determine the total amount of O2 in blood by adding the amount bound to hemoglobin and the amount in solution.

51
Q

Factors affecting binding of oxygen to hemoglobin

A

CO2, H+ and DPG all bind to hemoglobin and shift the curve to the right. Hb affinity for oxygen decreases.

Fetal hemoglobin: shift the curve to the left, so saturation of hemoglobin happens at a lower partial pressure of oxygen.

CO: Binds to Hb stronger than oxygen and has the same effect as having less Hb. Reversible binding but half-life is 4-6 hours. When a patient has CO poisoning give pure oxygen at the hospital to competitively lower CO half-life. Hb is already saturated so you are not trying to add oxygen to Hb.

52
Q

Transport of CO2

A

Can exist in solution, bound to Hb or as HCO3- Conversion to HCO3- is through carbonic anhydrase in red blood cells

53
Q

Rhythm regulation of breathing

A

regulation in the medulla

54
Q

Rate regulation of breathing

A

Central chemoreceptor: strongest effect. Neurons are located in the medulla. Responds to changes in PaCO2 (partial pressure of carbon dioxide in the arterial blood).

Peripheral chemoreceptor: afferent neurons in the carotid and aortic bodies. Two situations in which it is important in breathing:

  1. when PaO2 falls below 60 mm Hg which occurs in a variety of respiratory disorders and at high altitude
  2. With an increase in H+ which occurs at the lactate threshold (anaerobic threshold)
55
Q

Oxygen therapy

A

Given when PaO2 falls below 55 mm Hg. However if a respiratory problem involves a shunt, oxygen therapy is usually not useful. A shunt is where some of the blood from the pulmonary artery flows through a region of the lung that is not ventilated, and thus the blood is less oxygenated when leaving the lung.

56
Q

Low PO2

A

high altitude. formation of acute mountain sickness during rapid ascent. Thought to occur because of brain swelling which would result from hypoxia leading to vasodilation of blood vessels. Respiratory alkalosis also occurs. Reasoning has to do with peripheral chemoreceptor

57
Q

High PO2

A

Doesn’t really change anything.

58
Q

Effect of lactic acid on regulation of breathing

A

exercising. As you reach the lactic threshold Ve increases dramatically, PaCO2 goes down and PaO2 increases. Produce respiratory alkalosis (through decreased CO2 think of the chemical equation equilibrium if you remove CO2) to compensate for metabolic (lactic acid) acidosis.

59
Q

College student vs olympic athlete values

A

Similar values: maximum ventilation, arterial O2, arteril-venous O2 difference, maximum heart rate.

Different values: VO2 max due to increased maximum cardiac output and stroke volume.

60
Q

Kidney homeostasis in volume of ECF

A

Done by regulating the amount of sodium in the body.
Negative feedback loop: Disturbance to volume is detected by volume sensors that send a message to the effector system, which is the kidney.

If there is a loss of ECF, kidneys will save sodium.

If there is excess ECF, kidneys will excrete sodium.

Blood volume and ECF volume are closely related because ECF contains blood plasma.

Dis-regulation of ECF in hypertension and congestive heart failure. Often treated with diuretic which targets sodium.

61
Q

Kidney homeostasis in osmolarity of ECF

A

concentration of water. high osmolarity is a low concentration of water.

Disturbance detected by osmo-receptors that send a message to kidney to either save water (high osmolarity) or excrete water (low osmolarity).

When save water you are producing concentrated urine. Conversely, when you excrete more water you are producing dilute urine.

pH: Kidneys are long-term regulators. (Respiratory is short term). Protein concentrations will be effected by pH.

composition: other ions, waste, etc…. K+, Ca++,

62
Q

kidney functions: excretion

A
  1. metabolic wastes: Nitrogenous wastes including urea (by-product of metabolized amino acids), uric acid (by-product of metabolized nucleic acids), creatinine (muscle metabolism)
  2. foreign chemicals: xenobiotics.
    Collaboration with liver which makes molecules more soluble and capable of elimination through kidney.
  3. regulatory molecules: Including hormones.
63
Q

Kidney functions: endocrine

A
  1. erythropoietin: red blood cell production produced in kidney. Less produced in renal disease.
  2. renin: released from kidney in response to decreased renal perfusion. Activates angiotensinogen to angiotensin I which is converted to angiotensin II through ACE which is responsible for expanding ECF. Angiotensin II also stimulates release of aldosterone which acts in the kidney to increase sodium reabsorption to expand ECF volume. In chronic kidney disease, renin secretion increases.
  3. active form of vitamin D: also called calcitriol and is converted with regulation in kidneys. Levels decrease in chronic kidney disease.
64
Q

Renal Corpuscle of kidney

A

All in cortex
Glomerulus is the tough of blood capillaries
Bowman’s capsule: encases the glomerulus
Bowman’s space is between glomerulus and the capsule.

65
Q

Renal tubule structure

A

Lined with simple epithelium.
Begins where the Bowman’s capsule opens up at one end
Proximal Tubule: in cortex. Links to the loop of Henle.
Loop of Henle: in medulla
Distal Tubule: connects to the collecting duct into the papilla and is where the urine drains from. in cortex
Collecting duct: both medulla and cortex

66
Q

Blood flow to the nephron

A

Blood comes from the afferent arterioles then to the glomerular capillaries and then blood leaves the glomerular capillaries via the effferent arteriole.

Vasa recta: capillaries that flow in parallel to the Loop of Henle. Located in medulla.

Peritubular capillaries: located in cortex.

67
Q

Nephron: Filtration

A

initial very non-specific process that eliminates based on size (smallest eliminated).

Occurs in the glomerulus (renal corpuscle) and is pushed into Bowman’s space.

Filtrate then flows through renal tubulars.

Examples of small molecules include glucose, amino acids, ions, peptides, drugs and waste products of metabolism.

68
Q

Nephron: Tubular reabsorption

A

Bring back into body, from lumen of tubule and into ECF. Can happen in loop of Henle and collecting duct as well.

69
Q

Nephron: tubular secretion

A

Remove from body, from ECF and into the lumen of the renal tubular. Can happen in loop of Henle and collecting duct as well.

70
Q

Filtration membrane

A

Filtration = movement of substances from inside plasma to Bowman’s space. Passive of bulk flow (everything moves together) therefore the concentration of a substance inside the plasma will be the same concentration as in Bowman’s space.
Have to pass filtration membrane to flow into Bowman’s space.

71
Q

Cell types in the glomerulus

A
  1. fenestrated endothelial cells: lines glomerular capillary, has fenestrations (pores).
  2. podocytes: Surface of Bowman’s capsule that lines the capillaries. Inter digitating foot processes. Spaces between foot processes are called filtration slits. Slit diaphragm is a protein structure that is important for selectivity of flow.
  3. mesangial cells: connective-tissue type cell. gives structure to capillary loops.
72
Q

Glomerulus flow

A

plasma –> endothelium –> basement membrane (shared between endothelium and podocytes) –> filtration slits –> Bowman’s space

73
Q

Selectivity in glomerular filtration

A

Freely filtered: small molecules, water, ions, amino acids etc… Plasma concentration = concentration in Bowman’s space. Bulk flow.

Not filtered: cells, proteins

74
Q

Disorders of the filtration membrane

A

Proteinuria: when proteins get filtered and end up in urine. Hallmark of kidney disease.

Congenital proteinuria are babies whose filtration system never works properly. It is a rare genetic disorder affecting the proteins in the slit diaphragm.

75
Q

GFR

A

GFR is the rate at which plasma is filtered.

Typical for male is 130 mL/min and women is 120 mL/min.

Chronic Kidney disease is defined as a GFR less than 60 mL/min and anything lower is associated with an increased risk of death from cardiovascular disease.

76
Q

Measuring GFR

A

Can measure directly by measuring inulin clearance, however it must be infused and is normally not practical
In practice measure creatinine which is an endogenous product of metabolic breakdown in skeletal muscle
Creatinine clearance is used to estimate GFR and serum creatinine is used to monitor kidney function.

77
Q

Net filtration pressure

A
  1. Net glomerular filtration pressure is the sum of all pressures.
  2. Pgc is the pressure in the glomerular capillaries out of capillaries
  3. Pbs is the hydrostatic pressure in Bowman’s space. Into capillaries
  4. pie GC refers to osmotic pressure due to blood proteins. Into capillaries
  5. Pressure in glomerular capillaries is very high because blood leaving the glomerulus exits via the efferent arteriole which provides a lot of resistance creating high pressure.
78
Q

Three methods of regulation for GFR

A

renal autoregulation, sympathetic nervous system, atrial natriuretic peptide

79
Q

Renal autoregulation of GFR

A

Mechanism is intrinsic to kidney. If MAP changes within 80-160 mm Hg renal autoregulation counteracts through dilation or constriction of affferent arterioles. If MAP increases, afferent arterioles constrict to keep pressure in glomerulus constant and GFR steady. Affected in kidney disease.

80
Q

sympathetic nervous system regulation of GFR

A

Stress and when MAP drops below 80 mm Hg. Overrides renal autoregulation. Input to afferent arteriole to constrict and lower GFR. Works to save volume, like in a hemorrhage or dehydration.

81
Q

atrial natiuretic peptide regulation of GFR

A

Activated when MAP is too high, or when ECF increases. Increases sodium excretion (natriuresis) to increase GFR. Hormone released by cells in the heart.

82
Q

proteinuria

A

Key sign (medical observation) of glomerular disease. High levels of protein in the filtrate effects renal tubules and activates inflammatory responses. Ultimately, get cellular damage that leads to loss of nephrons and decreased GFR. Treatments that decrease proteinuria have renoprotective effects and block RAAS (ACE, ARBS, aliskiren which is a direct renin inhibitor). Use assay of albumin to determine proteinuria. High values is called albuminuria.

83
Q

Nephrotic syndrome

A

severe proteinuria defined as greater than 3.5 g/day. Also get abnormal sodium retention, edema, increased clotting and hyperlipidemia.

84
Q

End stage renal disease

A

need transplant or hemodialysis. Major culprit is diabetes mellitus, second is hypertension.

85
Q

Diabetes mellitus or insipidus and polyuria

A
  1. Both disorders cause polyuria, or excessive urine output. diabetes insipidus as a disorder of urine concentration and is discussed later.
  2. Normally 100% of glucose is reabsorbed through specific binding to cotransporters.
  3. With hyperglycemia, there is a high filtered load of glucose that exceeds the capacity of the kidney tubule reabsorption. Transport proteins become saturated and glucose is lost in the urine
  4. Glucose in the urine promotes water to enter through osmosis.
  5. SGLT2 inhibitors promote this process
86
Q

Diabetic nephropathy characteristics

A
  1. Leading cause of ESRD.
  2. Glomerulosclerosis: increased extracellular material, thickened basement membrane (but leakier), decreased surface area for filtration, decreased GFR.
  3. Loss and effacement (flattening) of podocytes
  4. Consequences are leaky filtration membrane which causes proteinuria and decreased GFR.
87
Q

Diabetic nephropathy pathogenesis

A

hyperglycemia and decreased insulin signaling causes abnormal glycosylation. In the kidney this causes abnormal signaling processes resulting in glomerulosclerosis. Some evidence that decreased insulin signaling and abnormal kidney signaling causes the podocyte effacement.

88
Q

Diabetic nephropathy treatment

A

blood sugar control, blood pressure control. Preferred drug of choice are ACE inhibitors, angiotensin II receptor blockers ARBs (target RAAS renin-angiotensin-aldosterone system). Also the direct renin inhibitor aliskiren.

Angiotensin II works on ECF but also has intrarenal effects which can make proteinuria worse. ACE and ARB are considered “renoprotective” because reduce proteinuria

89
Q

Glomerular disease: hypertension

A

Hypertension causes CKD (chronic kidney disease)
In CKD get increased renin secretion increasing angiotensin II which causes vasoconstriction and increases in ECF volume, which provokes hypertension.

90
Q

glomerular disease: preeclampsia

A

occurs in pregnancy.

VEGF: vascular endothelial growth factor that is necessary to maintain endothelial cells.

increased vascular tone: smooth muscle cells contracting. Generalized constriction.

glomerular endotheliosis: swollen glomerulus and very constricted capillary loops

91
Q

Glomerular disease: glomerulonephritis

A

acute or chronic inflammation damaging the filtration membrane.
Hematuria is a characteristic and is blood in the urine.
Causes: SLE (systemic lupus erythematous), IgA nephropathy
Treatment: immunosuppressive drugs, in particular glucocorticoids.

92
Q

Reabsorption of organic molecules in kidney

A

Occurs in proximal tubule.
hyperglycemia can saturate renal glucose transport and cause polyuria.
Reabsorption is mediated by SGLT2 protein. Which is the sodium glucose co-transporter.
Drugs that block SGLT2 transporter: reduce hyperglycemia, promote weight loss and reduces glucose that is independent of insulin.

93
Q

Secretion of organic molecules in kidney

A

tubular secretion is open to competitive inhibition
proximal tubule. Lots of mitochondria.

94
Q

Locations of sodium reabsorption in the nephron

A

proximal tubule, ascending loop, distal tubule, cortical collecting duct

95
Q

Sodium reabsorption in the proximal tubule

A

co-transport with organic molecules. Absorption. Accounts for 65%-70% of sodium reabsorption. Also accounts for water reabsorption due to osmosis.
counter-transport with H+

96
Q

sodium reabsorption in the thick ascending loop

A

Cuboidal epithelium makes up thick segment.

Accounts for about 25% of sodium reabsorption.

Na gradient determines movement. Active process.

Na, K and 2 Cl in.

Blocked by loop diuretics furosemide or bumetanide. Diuretics increase urine flow by having more sodium in renal tubule heading toward urine. As a solute water follows.

97
Q

sodium reabsorption in the distal tubule

A

About 5% of sodium reabsorption.
Cotransporter of Na and Cl.
Blocked by thiazide diuretic.

98
Q

sodium reabsorption in the cortical collecting duct

A

Na channel and linked potassium secretion.
About 2% of sodium reabsorption
Stimulated by aldosterone.
Regulated.
Na channel blocked by amiloride.

99
Q

Regulation of sodium reabsorption

A

Sensors include carotid baroreceptors, juxtaglomerular cells and macula densa and all increase renin secretions to increase ECF

100
Q

juxtaglomerular apparatus

A

regulation of sodium reabsorption

  1. Macula densa: sensor in distal tubule measuring amount of Na+
  2. Justaglomerular cells: responders in the afferent arteriole. Release renin. Renin stimulates aldosterone secretion through angiotensin II which stimulates sodium reabsorption in the cortical collection duct (saves sodium). Saving sodium increases ECV.
  3. Aldosterone is produced in the zona glomerulosa of the adrenal cortex.
  4. Activated in response to decreases in ECV.
101
Q

RAAS

A

renin-angiotensin-aldosterone system

Factors regulating renin release:

  1. lower Na+ in distal tubule. Sensed by macula densa. Decreases in ECF volume causes decrease in GFR. Slower flow and proportionally a greater amount of Na removed prior to the distal tubule. Activates juxtaglomerular cells through JGA.
  2. sympathetic nervous system: innervates afferent arteriole and can stimulate renin release. Causes afferent arteriole to constrict which lowers GFR and also it stimulates juxtaglomerular cells to release renin. We learned the lowering of GFR earlier with decreased MAP sensed by the carotid baroreceptors.
  3. decreased pressure in afferent arteriole: juxtaglomerular cells are intrarenal baroreceptors that release renin with lower pressure in afferent arteriole.
102
Q

Renovascular hypertension

A

Accounts for less than 5% of hypertension.
Narrowing of artery to kidney increases renin release
Renal artery stenosis.

103
Q

Water reabsorption along the nephron

A

Water permeability varies along the nephron.
non-regulated: proximal tubule (and structures in cortex)
regulated: medullary collecting duct. Regulated because it depends on the number of aquaporins in the membrane.

104
Q

Descending limb in loop of henle

A

permeable to water. Water leaves tubule because thick ascending limb is creating a hyper-osmotic environment. And solutes can’t leave the tubule so filtrate becomes more concentrated.

105
Q

Ascending limb in loop of henle

A

not permeable to water. Throwing out Na. Active reabsorption.

106
Q

Counter current flow in loop of henle

A

traps osmolarity at bottom of loop in medulla.

107
Q

vasa rectum and osmolarity in loop of henle

A

In medulla have vasa rectum which are in parallel to loops of henle. flow of blood is in same direction and plasma equilibrates with environment which enables blood flow to medulla without “washing away” hyper-osmotic gradient.

108
Q

Vasopressin

A

antidiuretic hormone regulates water permeability by increasing aquaporins (AQP2) in the apical plasma membranes of the collecting ducts.

On basolateral surface have a type of aquaporin that is always there.

AQP2 are held in vesicles within cells until vasopressin stimulates movement to apical surface.

109
Q

Regulation of vasopressin release

A
  1. Vasopressin is released from posterior pituitary (neurohypophysis) and is regulated by osmoreceptors, located in hypothalamus, and they sense change in ECF osmolarity.
  2. An increase in ECF osmolarity (dehydration) increases action potential firing in osmoreceptors which increases vasopressin secretion. Result is increased water permeability in medulla and increased water reabsorption.
  3. osmoreceptors also initiate stimulation of thirst.
110
Q

Diabetic insidpidus

A

major disorder involving water regulation.
main symptom is polyuria due to a defect in the ability to reabsorb water and concentrate urine..

Two types: two types central and nephrogenic.

111
Q

Central diabetes insipidus

A

deficiency of vasopressin. Treatment is vasopressin replacement.

112
Q

Nephrogenic diabetes insipidus

A

kidney doesn’t respond to vasopressin. Either is a mutation in vasopressin receptor or a mutation in AQP2.

Treatment: Can’t use vasopressin (obviously). Mainly is supportive therapy.

Lithium is known to cause acquired nephrogenic diabetes insipidus.

113
Q

Potassium in ECF

A

Only 2% is in ECF, mainly found within cells. The level of ECF potassium influences membrane potential so it is important to regulate the amount of ECF potassium. Especially affected is the heart.

hypokalemia: too low of ECF potassium levels
hyperkalemia: too high of ECF potassium levels

114
Q

Potassium regulation

A

Regulation through secretion in cortical collecting duct. Aldosterone regulates Na reabsorption and K secretion is linked.

115
Q

Potassium and loop and thiazide diuretics

A

loop diuretics and thiazide diuretics increase Na delivery to the cortical collecting duct (get more Na reabsorption) which increases K secretion.

Cause hypokalemia.

loop diuretics: block Na/K/Cl co-transporter.

thiazide diuretics: block Na/Cl co-transporter.

116
Q

Potassium sparing diabetics

A

amiloride blocks Na channel in cortical collecting duct. And aldosterone antagonists (spironolactone and eplerenone).

117
Q

Acid Base Regulation

A
  1. buffers
  2. respiratory compensation: CO2 + H2O –> carbonic acid –> H+ + HCO3-. If H+ increases then blow off more CO2 to remove H+.
  3. kidneys: long-term response to adjust ECF pH through bicarbonate reabsorption in the proximal tubule. Bicarbonate is an important buffer system. H+ secreted into lumen which reacts with HCO3- in lumen to give H2O and CO2 which freely diffuse into cell. Essentially then move bicarbonate from reverse reaction in cell into body. Example: have acidosis want H+ secretion > HCO3- filtered from blood. This will lead to increased HCO3- reabsorption to buffer low pH.
118
Q

Urination anatomy

A
  1. ureter: bringing urine from kidney to bladder in the trigone region. Behind bladder then enter at back wall of bladder and join in an oblique way which prevents urine reflex.
  2. detruser muscle: walls of bladder (smooth muscle) lined by uroepithelium.
  3. urethra: bladder outlet
  4. internal urethral sphincter at neck of bladder which is a thickening of the smooth muscle.
  5. external urethral sphincter of skeletal muscle on the pelvic floor.
119
Q

Neural control of urination

A
  1. parasympathetic neurons stimulate contraction of the detrusor muscle.
  2. sympathetic neurons stimulate contraction of the internal sphincter.
  3. somatic efferent neurons stimulate contraction of the external sphincter.
  4. bladder afferent neurons in wall of bladder sense fullness as bladder fills which sends urge to urinate to the brain.
120
Q

Regulation of urination

A

storage of urine (as bladder fills): parasympathetic is inhibited, sympathetic and somatic are stimulated.

elimination of urine: parasympathetic is stimulated and sympathetic and somatic are inhibited.

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