Patho exam 1

 

 

Pathophysiology

Study Guide for Exam 1

 

A)   Terminology

 

1.     Know the definition of:

□  Pathophysiology – the science that studies the process of a disease or abnormal events affecting cells, tissues, organs, or the entire body.

□  Know the main topics discussed in general pathophysiology.

□  Pathology- Investigating changes in the body to help identify causes of the disease. The changes studied include:

-        Taking a biopsy and studying the cells under a microscope to determine the stages of cacer.

-        Looking at an organ post-mortem and studying it’s appearance.

-        Using immunological (serological) methods to make evident changes in cells and organs.

-        Autopsy to determine cause of death.

□  Etiology- Study of the cause of disease.

2.     Know the definition of disease. List at least one example for each of the following etiologies:

□   Infection- bacteria, viruses, fungi, parasitic worms.

□   Heredity- inherited, Ex: muscular dystrophy, cystic fibrosis.

□   Malnutrition- Ex: Scury caused by the absence of Vitamin C in food.

□   Immunity- The immune system attack the the hyaline cartilage of the joints. Ex- Rheumatoid arthritis (abnormal t cells).

□   Degeneration- Neurons die over time because of accumulation of abnormal proteins. Ex: Alzheimers disease.

□   Trauma- Physical (spinal cord injury) or psychological (posy traumatic stress disorder).

3.     Know the definition of idiopathic, teratogenic, iatrogenic, and nosocomial, and know at least one example for each of these types of diseases.

Idiopathic- The direct cause of the disease is unkown. Ex: Juvenile idiopathic arthritis- arthritis present in a child/young adult and there is no clear reason for disease.

Iatrogenic: Diseases that are associated with treatment or mistakes that doctors make. Ex: Asprin induced peptic ulcer- caused by damage and erosion of the stomach lining which is a side effect of medication on an empty stomach.

Teratogenic: Disease caused by either microorganisms or chemicals capable of causing damage to the fetus. Ex: If a pregnant women is infected with Zika virus, the fetus could be miceocephalic (smaller than normal brain).

Nosocomial: Infection contracted at a hospital or health care facility. Ex: MRSA (Methicillin Resistant Staph. Aureus).

4.     Know the main difference(s) between an acute and a chronic disease.

Acute: Rapid onset, brief course- a cold, influenza, food poisoning.

Chronic: Slow onsetm long course- HIV/AIDS, heart failure, hepatitis B and C infections, chronic kidney disease.

5.     Please remember that clinical manifestation is another term used for signs and symptoms of a disease.

6.     Be able to differentiate between a sign and a symptom.

Signs: alterations observed or measured by another person objectively. Ex: Pulse, BP, body temp, respiratory rate, lab findings, systemic changes.

Symptoms: Subjective experience reported by patient, Ex: Pain, nausea, dizziness.

7.     Differentiate between local and systemic (these are signs and symptoms affecting the entire body) signs of a disease.

Local changes: Redness, swelling.

Systemic changes: Fever.

8.     Know the vital signs.

Pulse rate, blood pressure, body temperature, respiratory rate

9.     Know the definitions of:

□   Diagnosis- Identifying the specific disease. Can use a blood/urine analysis, imaging, or immunology.

□   Treatment- Therapy to cure or reduce clinical manifestations.

□   Remission- No visable evidence the disease is progressing.

□   Exacerbation- Sudden increase in the severity of the disease

□   Prognosis- Expected outcome of the disease.

□   Complications- Unfavorable conditions that arise in the course of a disease. Ex: A complication of diabetes mellitus is blindness.

□   Sequelae: Permanent changes agyer the disease is cured.

10.  List some laboratory tests and imaging procedures that aid in diagnosis.

-        Blood analysis

-        Urine analysis

-        X-ray

-        Ultrasound

-        CT scan

-        Immunology

11.  Know the stages of the disease process using an infectious disease process as an example.

First is the latent period, where the pathogen begins replicating but is not yet contagious. Next is the incubation period, which is the time between exposure to the pathogen and the first appearance of symptoms. This is followed by the prodromal period, where mild, non-specific symptoms like fatigue or a slight fever begin. The invasive period comes next, marked by the most severe symptoms as the infection peaks. Finally, the convalescent period occurs as the body recovers and symptoms subside, leading to eventual health restoration.

12.  Know the definition of:

□   Epidemiology- the science of tracking patterns of transmission of diseases.

□   Prevalence- The number of existing cases in a population.

□   Incidence- The number of new cases within a period in a population.

13.  Know the importance of knowing the risk factors (or predisposing factors) and the precipitating factors for certain diseases.

Knowing risk factors can help public health officials make reccominations on how to reduce the risk of diseases.

14.  Know the definitions for epidemic, pandemic, sporadic and endemic diseases.

Epidemic: An increased number of diseased people within a specific population.

Pandemic: Disease present throughout the world often in increasing numbers.

Sporadic: A disesse occurring in low numbers and no pattern.

Endemic: A disease that is present in a specifc geographical area.

 

                       

 

 

 

B)    Regulation of Fluid Balance

 

 

1.     Know the two main compartments of Total Body Water - ICF and ECF

Intracellular fluid: Inside the cell; 40% body weight

Extracellular fluid: Outside of the cell; 20% body weight. Divided into interstitial fluid (80% of ECF) and plasma volume (20% of ECF).

2.     Know the sub compartments of ECF – plasma, interstitial fluid, and the smaller cavities. This last one is important when we talk about the third spacing – which describes the accumulation of fluid in cavities that are not as easily accessible as a source of fluid. For example: ascites will cause a person to have a lot of fluid accumulated in the peritoneal cavity, but this person may have decreased blood pressure.

Interstitial fluid: Fluid that fills the interstitial space or the space between the cells and the capillary that serves them.

Intravascular fluid or plasma: fluid that fills the vascular system (blood vessels).

Transcellular fluid: filling smaller cavities such as pleural, peritoneal, pericardial, cerebrospinal, synovial etc.

3.     Know the location of the pericardial, pleural, and peritoneal cavities

Pericardial- surrounds the heart in thoracic cavity.

Pleural- surrounds lungs in thoracic cavty.

Peritoneal- surrounds abdominal organs in abdominal cavity.

4.     Know the factors that would affect the percentage of water content in a human body- sex, age, percentage of body fat.

Sex

Men- Higher water percentage and lower proportion of body fat

Women- Lower water percentage and higher proportion of body fat

Age

Infants- Highest water content and less fatty.

As you age, water body content decreases.

5.     Know the reasons why infants and young children are more susceptible to dehydration and know some signs of dehydration.

Infants are very susceptible to dehydration because they are losing more water than their total body weight. Some signs of dehydration are dry mouth/tongue, few or no tears, sunken fontanelle, sunken eyes and cheeks.

6.     Know several reasons why aging can affect fluid balance.

Increases adipose and decreases muscle tissue

Decreases thrist sensation

Reduced kidney function

Reduced total body water

7.     Know the fact that water moves freely across the plasma membrane via aquaporins.

8.     Water movement across the membrane aka osmosis occurs down the concentration gradient that is why it is important that the ECF and ICF should be isosmotic/isotonic.

9.     Know the pathway of fluid movement when we have diarrhea – the diagram (or figure) we discussed in class. There might be a figure like that in the exam.

10.  Know the main sources of water intake/gain.

Water gain: Food, drink, and metabolism.

Water loss: Skin, lungs, urine, feces.

11.  Know the main routes of fluid loss – please remember that only urine volume is regulated based on fluid balance and blood pressure. Please make the connection that increased urine volume increases fluid loss and decreased urine volume is associated with decreased fluid loss/fluid retention.

12.  Know the thirst mechanism – stimuli, function, and result – this is a negative feedback mechanism

Stimuli: Increased blood osmolarity, decreased blood volume/pressure.

Function: Restore fluid balance by promoting water intake.

Result: A negative feedback loop that corrects dehydration and maintains homeostatis.

13.  Know the definition for hypodipsia.

14.  Reduced or absent sensation of thirst when the body requires fluid. Damage to hypothalamus, normal with age.

15.  Know the definition of polydipsia and remember this: there is an increased thirst associated with conditions such as increased plasma osmolarity, decreased blood pressure, dehydration, hypovolemia, etc. Another example - the abnormal sensation of thirst called psychogenic polydipsia is often observed in patient with schizophrenia.

Excessive thrist- when hydration levels are normal but person is thirsty

16.  Know the main stimuli for increased ADH secretion.

Increased plasma osmolarity

Decreased blood volume or pressure

17.  Know the mechanism of action of ADH – increased permeability of collecting duct via insertion of aquaporins. Increased ADH will increase water reabsorption in the collecting duct of the kidney tubule.

18.  Please make the connection between increased ADH levels, and decreased urine volume.

Increased ADH levels cause the kidneys to reabsorb more water, leading to decreases urine volume.

19.  Define diabetes insipidus, some causes (neurogenic vs nephrogenic) and some of its manifestations.

Increased urine fluid loss because of increased urine volume.

Neurogenic: decreased ADH secretion- head trauma near the hypothalamus.

Nephrogenic: decreased response to ADH by kidneys- pyelonephrisis.

Manifestations: Increases urine output, diluted urine, increases thirst.

20.  Define SIADH and know at least one cause for the acute/temporary form.

Syndrome of inappropriate ADH secretion- abnormally increases ADH secretion

Acute: head trauma

Chronic: CNS tumors, HIV infection

Manifestations: Low plasma osmolarity, decreased urine output.

21.  Know the two main reasons for the chronic form of SIADH:

□   Paraneoplastic syndrome - specific tumors such as bronchogenic carcinoma secretes ADH-like molecules and this secretion does not “obey” the normal negative feedback, so we have abnormal retention of water.

□    HIV infection

22.  Explain why hyponatremia is the most common finding in patients with SIADH

Too much ADH makes the body hold onto water, which dilutes the sodium in the bood.

23.  Remember that capillaries are the exchange vessels – their wall is thin and there are openings between endothelial cells - this will allow movement of water, ions, and small molecules out of and into the capillary – from the interstitial space. Red Blood cells and plasma proteins are not supposed to pass through.

24.  Know the main forces influencing capillary exchange or filtration. (Starling forces).

Inside the capillary

1.     Capillary hydrostatis pressure (hp)- forces fluif out of capillary.

2.     Capillary oncotic pressure (op)- pulls fluid back into the capillary.

Outside the capillary

1.     Intersitial fluif hydrostatic pressure

2.     Intersitial fluid oncotic pressure

The direction of fluid movement will be determined by the difference between these two opposing forces-Hp and Op

25.  Know the direction of fluid movement in the arteriolar end and venous end of a capillary (difference between the capillary hydrostatic pressure and capillary osmotic/oncotic pressure).

Arteriolar end: Hp is greater and fluid moves out of the capillary.

Venous end: Op is greater and fluif movies into the capillary.

26.  Know the role of lymphatic capillaries in removing some fluid from the interstitial space and where does the fluid (lymph) return.

They absorb excess fluid from the intersitial space to prevent swelling and transport it as lymph. It eventually returns to the bloodstream through the subclavian veins.

27.  Define Edema.

Abnormal accumulation of fluid within the intersitial spaces.

28.  Know why increased venous pressure will cause edema and illustrate it in the case of CHF.

Increased venous pressure slows blood return to the heart causing fluid to back up and leak into the tissues, leading to edema. In congestive heart failure, weakened heart function increases venous pressure, causing peripheral edema and pulmonary edema, leading to swelling and difficulty breathing.

29.  Why will a decreased plasma protein concentration (hypoproteinemia) cause edema? Give at least two examples.

It reduces oncotic pressure, which normally pulls fluid into the bood vessels. Without enough proteins, fluid stays in the tissues causing edema. Examples are liver disease and kidney disease.

30.  Know the two main reasons for ascites in a patient with liver failure.

1.     Decreased levels of albumin in plasma

2.     Portal vein hypertension

31.  Why will a damaged or obstructed lymphatic vessel /lymph node cause edema? Give two examples.

Damage or obstructed lymphatic vessel prevents proper drainage of excess fluid from the intersitial space.

Example: Damage from surgery or a parasitic infection.

32.  Know two reasons for increased capillary permeability and why this will be accompanied by edema.

1.     Allergic reactions- histamines released makes capillaries more permeable and allows fluid and proteins to leak into tissues

2.     Inflammation caused by trauma/injurt and infection- Damage to capillary walls increases permeability, leading to fluid leakage causing edema.

33.  Know the difference between pitting and non-pitting edema.

Pitting: Press on swollen area and it leaves a dent. Common in heart, kidney, or liver disease.

Non pitting: Press on swollen area and it doesn’t dent. Common in lymphedema and hypothyroidism.

34.  Give at least two examples of acute/life threatening edema.

1.     Pulmonary edema: fluid buildup in lungs and low oxygen levels.

2.     Cerebral edema: Swelling of brain due to trauma, stroke, infection, tumors.

35.  Give at least two reasons why chronic edema is detrimental to tissues.

1.     Poor blood flow

2.     Long term swelling causes tissue damage

 

C)   Electrolyte Imbalances – Regulation of Sodium in plasma

  1. Know the sources of intake and loss for Na ions - it is important to remember that sodium ions are most concentrated in the ECF, and they are the major contributor to plasma osmolarity (concentration)

Intake: Food and beverages

Loss: Urine, sweat, feces

  1. Remember that only sodium loss is regulated, and that regulation happens as part of the regulation of blood volume and pressure.

  2. Review - Know the definitions for reabsorption and secretion at the kidney tubule – just a review to help you with understanding the actions of hormones.

 

  1. Know the meaning of the baroreceptor reflex and its response(s) when BP decreases or increases - the concept map in the lecture.

A fast response initiated by an immediate change in blood pressure in larger blood vessels closer to the heart.

A decrease in BP will cause the stimulation of the SNS and inhibition of the PNS. As a result, heart rate, stroke volume, and peripheral resistance will increase.

An increase in BP will cause the inhibition of the SNS and the stimulation of the PNS. As a result, heart rate, stroke volume, and peripheral resistance will decrease.

  1. Review the action of SNS on the smooth muscle of peripheral arterioles – peripheral vasoconstriction when SNS is activated. Remember that peripheral vasoconstriction would increase peripheral resistance, and this will contribute to maintenance or increase in MAP (BP).

 

-        Norepinephrine is released and binds to alpha-1 receptors on smooth muscle in peripheral arterioles.

-        This causes the smooth muscle to contract, leading to vasoconstriction (narrowing of blood vessels).

-        Vasoconstriction increases peripheral resistance, which helps maintain or raise blood pressure (BP).

 

  1. To remember: CO (cardiac output) depend on the product of Heart Rate and Stroke Volume

  2. To remember - MAP (Mean Arterial pressure) depends on Cardiac Output (Heart Rate x Stroke Volume) and Peripheral Resistance.

  3. Know some signs present in people with increased stimulation of SNS – these signs would be more pronounced when BP levels would be low to very low such as in a person during a Myocardial Infarct (a heart attack) because of reduced stroke volume. Another instance of strong stimulation for SNS is hypoglycemia (reduced blood glucose levels).

Pale skin, increased heart rate, increased respiration, sweating and clammy skin.

  1. Know the mechanism of regulation blood volume and pressure when it decreases – RAAS (Renin Angiotensin Aldosterone System) – The stimulus, the sequence of events and the result.

Renin splits angiotensinogen and angiotensin 1 is formed. ACE splits angiotensin 1 and angiotensin 2 is formed

Stimulus: Decreased MAP. Decreased blood flow to the kidney causes in increase in renin release.

Result: Increased blood pressure

  1. Please remember the specific roles of angiotensin II

Stimulates ADH release

Stimulates aldosterone release

Stimulates thirst

Causes peripheral vasoconstriction

  1. Know the specific role for aldosterone (a sodium ion is reabsorbed while a potassium ion is secreted – this happens at the distal tubule).

Retain sodium and water, Increase blood pressure and volume.

  1. Know the mechanism of regulation blood volume and pressure when it increases – the stimulus for the increased secretion of ANP (Atrial Natriuretic Peptide), and its specific role.

Stimulus: Increased blood volume, increases stretch of atrial walls, atrial myocardiocytes.

Role: Stop sodium reabsorption, decrease RAAs activity, vasodilation of peripheral arteries.

  1. Differentiate between isotonic, hypotonic, and hypertonic alterations based on the concentration of plasma sodium.

Isotonic: No change in sodium concentration in ECF.

Hypertonic: Increased sodium concentration in ECF.

Hypotonic: Decreased sodium concentration in ECF

  1. Know: Normal Na+ levels in plasma – 135-145 mEq/L

  2. Define an isotonic alteration, plasma osmolality remains within normal range – 280-290 mOsm.

Water and electrolytes are lose in isotonic proportions.

  1. Give at least three causes of isotonic fluid loss (hypovolemia) and at least three signs and symptoms(for example – the person will be thirsty because of activation of thirst center via AII.

-        Loss of GI tract fluids (vomiting and diarrhea).

-        Excessive fluid loss at kidney (untreated diabetes mellitus)

-        Third spacing- ECF is trapped in a cavity or on the surface of the body (extensive 3rddegree burns).

Signs and symtoms

Weight loss, increased thirst, decreased urine volume.

17.  Know the definition of hypovolemic shock.

A life threatening condition caused by severee fluid loss, leading to low blood volume, poor circulation, and organ failure.

18.  To make a connection with the previous unit, third spacing is also a reason for hypovolemia. For example, a patient with ascites could have hypovolemia because the volume trapped in the peritoneal cavity will not be able to return to plasma and this cannot contribute to its volume.

19.  Give at least three causes of isotonic fluid gain/hypervolemia.

-        Renal failure

-        Iatrogenic

-        Hormonal

Signs and symptoms

Weight gain, distinction of neck veins

Edema causes by an increase in hydrostatic pressure

20.   List and explain at least two signs and symptoms and the reason (increased Hp) for edema.

High pressure in blood vessels pushes fluid out into tissues, causing swelling.

Signs and symptoms: Swelling and weight gain.

21.  Define a hypotonic alteration – plasma osmolarity decreases below the normal range of values – most often present as hyponatremia.

Plasma sodium concentration is less than 135 mEq/L

22.  Know at least two reasons for hyponatremia, describe its effect on cells and some clinical manifestations.

-        Loss of sodium in excess of water.

-        Gain of water in excess of sodium.

Hyponatremia decreases the ECF osmolarity and water moves out of the cell through osmosis, cells swell.

Manifestations

-        Headache, disorientation.

-        Muscle cramps, weakness, fatigue

-        GI issues- abdominal cramps, nasea, vomiting

23.  Define a hypertonic alteration – increased plasma osmolality above normal range of values – most commonly caused by hypernatremia.

Occurs when plasma sodium concetration is above 145 mEq/L.

24.  Know at least two causes for hypernatremia, describe its effect on the cells and some clinical manifestations.

- Insufficent water intake

- Excessive water loss

- Iatrogenic

Water movment from the ICF to the ECF- cells volume decreases, intracellular dehydration follows.

Manifestations

- Headache, disorientation, seizures, coma, death.

-Thirst, dry skin, and mucous membranes.

D. Electrolyte Imbalances - Potassium

 

25.  Know the importance of potassium in a human body: it is especially important to know its effect on the resting membrane potential and heart function.

a.     Resting membrane potential

b.    Action potential in the neurons- repolarization and hyperpolarization.

c.     Normal cardiac rhythm. Ex: rate of firing of the SA node

d.    Action potential in skeletal and smooth muscle.

e.     Can be exchanged with hydrogen across plasma membranes.

26.  Know the normal range for plasma potassium levels.

3.5-5.5 mEq/L

27.  Know several factors that would influence plasma potassium levels:

□   Role of Aldosterone- Determine the amount of potassium secreted in the urine. When plasma K+ levels increase and BP decreases, aldosterone secretion increases. Increases aldosterone levels cause an increase in K+ secretion at the kidney tubule.

□   Role of insulin- Increase potassium entry into the cells (ICF) after a meal.

□   Catecholamines- Stimulation of potassium entry into the cells (ICF).

□   Acute acidosis- Causes hyperkelmia

□   Acute alkalosis- Causes hypocalemia

28.  Define hypokalemia, list, and explain the reason for hypokalemia in:

Occurs when plasma potassium levels decreases below 3.5mEq/L

□   Reduced intake – the cause is limited diet

□   Increased loss of potassium – please remember that loss of GI fluid causes hypokalemia because of activation of RAAS.

□   Increased entry of potassium into cells: Iatrogenic means it happened because of the treatment of DKA

29.  Know the effect of hypokalemia on the membrane potential of excitable cells – muscle (skeletal, cardiac, and smooth) and neurons – especially peripheral nerves.

Low potassium makes cells too negative, which messes up their ability to send signals. This causes problems like muscle weakness, irregular heartbeats, and nerve issues.

30.  List and explain the clinical manifestations of hypokalemia.

a.     Skeletal muscle weakness

b.    Shallow respiration

c.     Decreases bowl motility

d.    ECG changes- slightly prolonged PR interval

e.     Dysrhythmias

31.  Define hyperkalemia and know the most common causes.

Occurs when plasma potassium levels increase above 5.5 mEq/L

Causes: Decreaaes renal secretion, release of K out of cells to plasma, addisons disease.

32.  Know and explain the effect of hyperkalemia in muscles and neurons.

Inititally, the cells would be more excitable because the resting membrane potential becomes less negative. As hyperkalemia continues, the nerves and muscle would become less responsive because it will be harder to start a new action potential.

33.  Differentiate between initial and late/severe clinical manifestations of hyperkalemia.

Initial: Tingling of lips and fingers, restlessness, intestinal cramping.

Late/severe: Weakness and loss of muscle tone iin skeletal muscle, bradycardia and cardiac arrest.

34.  Explain the rationale of the emergency treatment for hyperkalemia.

IV insulin and glucose, then dialysis.

E. Electrolyte Imbalances - Calcium

 

35.  Know the importance of calcium ions in several processes within the human cells.

Structure of bones and teeth, blood clotting, hormone secretion, transmission of nerve impulses, muscle contraction, heart rate and strength of contractions.

36.  Know the normal range for plasma calcium levels.

9-10.5mg/dL

37.  Know the three sites in the body that are important in the homeostasis of calcium.

a.     Bones ans teeth- storage site

b.    Duodenum and jejunum- absportion site

c.     Kidneys- excretion or reabsorped

38.  Explain the negative feedback between decreased plasma calcium levels and PTH. Know how PTH increases calcium levels.

Decreased calcium ion levels in the plasma will cause an increase in PTH secretion.

1.     Increase bone resorption through activation of osteoclasts.

2.     Increasing tubular reabsorption at kidney

3.     Increasing intestinal absorption from food through vitamin D activation.

39.  Define hypocalcemia.

Calcium levels in plasma under 9mg/dl

40.  List and explain the causes of hypocalcemia described in the lecture.

Hypothyroidism- low levels of PTh will cause calcium levels to decrease

Vitamin D deficiency-decreased calcium absorption

Inadequate intestinal absportion (Chrohns disease)

Nutritional defiencies

41.  Know some clinical manifestations of hypocalcemia.

Tingling, muscle spasms, intestinal cramping, hyperactive bowel sounds.

Severe: Convulsions and cardiac arrest.

42.  Remember that severe hypocalcemia can be identified by the Chvostek and Trousseau signs.

43.  Define hypercalcemia

Calcium levels in plasma over 10.5 mg/dl

44.  List and explain the causes of hypercalcemia described in the lecture.

Primary hyperparathyroidism- increased PTH levels would increase calcium levels

Renal failure- Not as much plasma is lost in urine and it accumulates in the plasma.

45.  Know that metastatic cancer cells can cause hypercalcemia directly (metastases) and indirectly by secreting PTH-like molecules (paraneoplastic syndrome).

46.  List and explain several clinical manifestations of hypercalcemia

Heart: dysrhymias, bradycardia, cardiac arrest

Central nervous system: confusion, depression, coma

Weakness, anorexia, constipation

Chronic: bone pain, osteoporosis

47.  Know the definition and the reason for metastatic calcification.

Hardening and organ damage from calcium salt deposition.

 

F. Alteration of plasma pH – simple acid base imbalances

 

48.  Know the importance of pH in the human body.

-        Changes shape of proteins

-        Affects nervous system

-        Plasma K+ and Ca distrubances

49.  Know the normal plasma pH values.

7.35-7.45

50.  Know the meaning and the values of acidosis and alkalosis.


51.  Know at least two sources of H+ in plasma under normal conditions

Carbonic acid formation, metabolic acids produced during normal metabolism.

52.  Know the role (and how it functions) of the bicarbonate buffer system.

Tie up the free hydrogen in the case of acidosis: H+ is higher than normal

Replenish needed free H+ in the case of aklalosis: H+ is lower than normal.

53.  Know the mechanism through which the respiratory system regulates the pH of plasma.

A decrease in plasma pH (too many H+) will stimulate chemoreceptors and induce hyperventilation (increased RR and depth) to have less CO2 and H in plasma.

An increase in plasma pH (not enough H+) will inhibit the chemoreceptors and induce hypoventilation (a decrease RR and depth) to have more CO2 and H+ in plasma.

54.  Know the renal mechanisms/responses for the regulation of pH of the plasma.

Normally, kidney cells secrete H+ and reabsorb bicarbonate ions. In acidosis, the kidneys secrete more H+ and produced new bicarbonate. In alkalosis, kidneys can secrete bicarbonate and reabsorb H+.

55.  Know at least two causes of respiratory acidosis and the compensatory responses.

Acute disorders of ventilation- pneumonia, asthma. No time for real compensation

Chronic disorders of ventilation- chronic obstructive pulmonary disorder. Compensation will occur by the kidneys reabsorbing more bicaronate ions.

Increased production of CO2- fever and sepsis.

56.  Know at least two causes of respiratory alkalosis and the compensatory responses.

Increased ventilation- anxiety attack

Improper use of medical ventilation

Kidneys will compensate by secreting bicarbonate in urine.

57.  Know at least two causes of metabolic acidosis and the compensatory responses.

Increased production of metabolic acid

Increased bicarbonate loss

Decreased renal function

Compensation: Hyperventilation will occur

58.  Know at least two causes of metabolic alkalosis and the compensatory responses.

Loss of stomach acid

Hypokalemia caused by excessive loss of potassium in urine

Hypoventilation will occur.