– steady state of internal balance, regulated by nutrient concentration, O2 & CO2, waste products, pH, water, salt & electrolytes, volume & pressure, temp

Question 1

Homeostasis

Answer 1

– steady state of internal balance, regulated by nutrient concentration, O2 & CO2, waste products, pH, water, salt & electrolytes, volume & pressure, temp

-disruptions results in illness, injury, lack of nutrients, infection
Feedback mechanisms

Question 2

Feedback mechanisms

Answer 2

oFeedback mechanisms have 3 components→
* Sensor mechanism(senses the disruption in Homeostasis)
*Control Center(regulates the response to the disruption)
* Effector Mechanism(acts to restore homeostasis)

• Negative: works to restore homeostasis by correcting disruption (Blood glucose levels)
• Positive: moves system further away from homeostasis ( intensifying labor contractions during birth)

Question 3

Altered Cell Function

Features of hypoxic cell injury

Answer 3

• Single most cause of cell injury
  -This is the decrease of Oxygen getting into the blood - cells(which is often caused by lung injury).

Question 4

Causes of irreversible cell injury

Answer 4

• Lysosomal membrane injury + leakage of toxic enzymes resulting in cell death
• Cell membrane damage CENTRAL FACTOR

Question 5

Causes of cellular swelling

Answer 5

-↓ ATP prod, impaired cell volume regulation, Na/K pump failure, intracellular Na+ accumulation

Question 6

Effectors of cell injury

Answer 6

• Oxygen &oxygen derived free radicals.
• Increase in cytosolic calcium & loss of homeostasis.
• ATP depletion
• Defects in membrane permeability

Question 7

(Inflammation)
Define nonspecific vs. specific immune responses

Answer 7

Nonspecific/innate
- Inflammation
- Natural barriers such as skin, epithelial membranes
Specific /acquired/adaptive
- Humoral immunity - B lymphocytes
- Cell mediated immunity – T lymphocytes.

Question 8

Describe components of the vascular response

Answer 8

• Vasodilation, ↑ vascuklar permeability, migration of WBC to injury site
• Plasma protein cascade, cellular elements, biochemical mediators
  Your components of the Vascular response are the Plasma Protein cascade(which consists of the complement system, the clotting system, and the Kinin system), the cellular elements(like your mast cells, your dendritic cells, leukocytes), and your mediators(such as Cytokines that are further divided into interleukins and interferons, and Chemokines which consist of Peptides).

Question 9

Define chemotaxis

Answer 9

Directional movement of cells along a chemical gradient formed by a chemotactic factor;Chemotaxis is the movement of an entity or organism in response to a chemical stimulus.

Question 10

Describe the role of the following in inflammation:
Complement system = initial frontline, recruits WBC to injury site

Answer 10

• Fragmentation of complements components
• Vasodilation
• Increased vascular permeability
• Rapid mast cell degranulation
• Opsonization
• Cell lysis
  Can sometimes destroy pathogens directly; it causes fragmentation of complement components(like proteins), then there’s vasodilation, followed by increased vascular permeability, then rapid mast cell degranulation/destruction, chemotaxis of neutrophils/the neutrophils travel to the site, next comes opsonization(where pathogens are marked for phagocytosis), and then, finally, cell lysis(the breaking down of the cell membrane).
• Overall the Complement functions are: 1)Lysis 2)Chemotaxis 3)Opsonization

Question 11

Clotting cascade ( coagulation)

Answer 11

• forms fibrinous meshwork to prevent spread of infection
  - traps microorganisms & foreign bodies at site of inflammation
  - forms clot to stop bleeding & framework for future repair & healing

Question 12

Bradykinin:

Answer 12

product of kinin system that causes dilation of blood vessels, acts with prostaglandins to stimulate nerve endings and induce pain, smooth muscle cell contraction , increases vascular permeability and may increase leurkocyte chemotaxis

Question 13

Mast cells :

Answer 13

histamine release/inflammatory mediators

Question 14

-Dendritic cells:

Answer 14

antigen presenting & activates T cells; they act as messengers between the innate and adaptive immune systems.

Question 15

Leukocytes:Consists of Granulocytes, Monocytes/Macrophages, Lymphocytes
Neutrophils→ Involved with phagocytosis; the 1st WBCs to the scene; make up 60-70% of total WBCs
Eosinophils→ Responsible for Allergies and fighting parasites; control the mechanisms assoc. with Asthma
Basophils→ These are responsible for inflammatory reactions during the immune response; are involved in hypersensitivity reactions.
Monocytes/Macrophages→ migrate and differentiate into tissue macrophages for Phagocytosis
NK Cells→ Provides for direct cytotoxic activity against virus-infected cells and cancer cells
B-Cells→ Make antibodies
T-Cells→ Fight off infections, diseases, and help to boost the immune system

Answer 15

Leukocytes:Consists of Granulocytes, Monocytes/Macrophages, Lymphocytes
Neutrophils→ Involved with phagocytosis; the 1st WBCs to the scene; make up 60-70% of total WBCs
Eosinophils→ Responsible for Allergies and fighting parasites; control the mechanisms assoc. with Asthma
Basophils→ These are responsible for inflammatory reactions during the immune response; are involved in hypersensitivity reactions.
Monocytes/Macrophages→ migrate and differentiate into tissue macrophages for Phagocytosis
NK Cells→ Provides for direct cytotoxic activity against virus-infected cells and cancer cells
B-Cells→ Make antibodies
T-Cells→ Fight off infections, diseases, and help to boost the immune system

Question 16

-Natural Killer Cells:

Answer 16

Provides direct cytotoxic activity against virus-infected cells and cancer cells

Question 17

Fluid and Electrolytes
Compare osmosis vs. hydrostatic pressure

Answer 17

• Osmosis – movement of water down a concentration gradient, that is across a semipermeable membrane region of high-water concentration🡪 low water concentration
• Hydrostatic pressure _ mechanical force of water pushing against cellular membranes.

Question 18

Know the ion composition of cytoplasm (potassium) and the ECF (sodium)

Answer 18

• ICF: K+, ECF: Na+
• Na+, K+ and A-(proteins) are the major cations. Extracellularly/in the ECF, Na+ is the major cation at 150. Intracellularly/in the ICF, K+ is the major cation at 150. So, Sodium basically remains outside of the cell while Potassium is largely inside of the cell. Proteins tend to stay in the cell and never leave.

Question 19

Describe the role of aldosterone and ADH in water balance

Answer 19

Aldosterone
- Alters reabsorption of sodium & water by distal & collecting tubes of kidney
- Regulates secretion of potassium by distal tubules
- Prod. By adrenal glands
Antidiuretic hormone
- Controls water excretion in kidneys in response to increased osmolarity and decreased BP
- Secreted by hypothalamus and stores and released from post. Pituitary

Question 20

List the 4 problems that result in edema

Answer 20

↑ capillary permeability: inflammation/immune response
↑ capillary hydrostatic pressure: salt & water retention (CHF, RF, cirrhosis), venous obstruction
↓ capillary oncotic pressure: decreased production of plasma proteins (liver disease, protein malnutrition), loss of plasma proteins (nephrotic syndrome, hemorrhage, burns)

Question 21

Describe the causes of the following alterations in sodium and water balance:

Question 22

Compare the causes of hypokalemia/hyperkalemia and hyponatremia/hypernatremia

Question 23

*IMPORTANT NOTES:

Answer 23

Higher K+ = Higher acidity; Lower/Less K+ = Less Acidity
When you get too much water in the body, it causes this “watering down” effect where the excess water dilutes the sodium so much that it ends up making the amount of Na in the body seem like it’s low. Since the body is perceiving such a low amount of Na+, Hyponatremia ends up happening.

Question 24

Acid/Base Imbalances
Describe how acidosis can lead to hyperkalemia

Answer 24

↑ hydrogen secretion and ↓ K+ secretion ,= ↑ K+ retention. Acidosis can lead to hyperkalemia by causing a shift of potassium ions from inside the cells to outside of the cells. This shift occurs because of the increase in hydrogen ions in the extracellular fluid. The increase in hydrogen ions causes potassium ions to move out of cells and into the extracellular fluid. This shift can cause hyperkalemia.(Hyperkalemia is when you have more K+ in the ECF/body fluid and more H+ in the ECF/body fluid. If you remember, Hyperkalemia is when serum potassium is greater than 5.5. So, if more potassium is moving into the blood, because it’s following the H+, you’d get these higher K+ levels).

Question 25

Describe the 4 buffering systems in the body

Answer 25

Carbonic acid Buffer
changes brought about by causes other than fluctuation in CO2 generated H2CO2
– lactic acid, loss of HCL due to vomiting
Protein buffer
Primarily important intracellularly
Excellent because they contain both acidic/basic groups that can give/take up H+
Hemoglobin buffer- Most H+ generation from CO2 at tissue becomes bound to Hb
Phosphate buffer- Important intracellularly and in urine

Question 26

Define, state the etiology, pathophysiology, and compensatory mechanisms for (review the acid/base assignment):

Question 27

Cardiovascular Pathophysiology
Criteria for the metabolic syndrome

Answer 27

Increased waist circumference : men >40 in, Women >35 in
Plasma triglycerides ≥ 150 mg/dl
HDL-C : men <40, women <50
BP ≥130/85
Fasting plasma glucose ≥100 mg/dl

Question 28

Risk factors for coronary heart disease

Answer 28

Modifiable
Hyperhomocysteinemia, dyslipidemia
HTN, smoking, obesity, DM, sedentary lifestyle, stress, alcohol

Nonmodifiable

Increasing age, male gender/women after menopause, genetic predisposition, black/Asian

Question 29

Factors involved in the development of the atherosclerotic plaque

Answer 29

Initiating event – endothelial damage **
Oxidation of LDL is central to the development of atherosclerotic plaque
Injury to endothelium causing endothelial dysfunction & inflammation.
Inflammatory cytokines release 🡪 draw monocytes
Monocytes adhere to damaged endothelium, migrating between endothelial cells into intima.
Monocytes 🡪 macrophages releasing enzymes & toxic oxygen free radicals causing more damage leading to oxidation of LDL
Macrophages that engulf oxidized LDL🡪 foam cells🡪 fatty streaks

Question 30

Clinical manifestations of the different types of chest pain (e.g. stable angina, unstable angina, etc.)

Answer 30

Stable angina

Short lasting chest pain that many radiate , commonly mistaken for indigestion
-associated with pallor, diaphoresis, dyspnea
-caused by gradual luminal narrowing and hardening of arterial walls
-relieved by rest & nitrates

Prinzmental angina

Chest pain due to transient ischemia occurs exclusively at rest
-caused by vasospasm of coronary artery w/wo atherosclerosis
-cyclic pattern of occurrence
-results from hyperactivity of SNS, increased ca+ influx in arterial smooth muscle, impaired prod. Prostaglandin/thromboxane

Silent/asymptomatic

• presence of regional abnormality in left ventricular sympathetic afferent innervation
• metabolic dysfunction in DM
  -following CABG/cardiac transplant
  -following ischemic nerve injury by MI

Unstable angina

Reversible myocardial ischemia & is a harbinger of impending infarction.
-symptoms with no apparent trigger
-long duration and cannot be relieved by nitrates.
-caused by rupture of plaque in coronary artery

Question 31

Etiology and pathophysiology of right-sided and left-sided heart failure

Answer 31

Left Sided HF

Systolic/diastolic ventricular dysfunction
↓ left ventricular emptying & abnormal diastolic relaxation
↑ volume & pressure in left ventricle, atrium
↑ volume in pulmonary veins & pulmonary capillary bed
Pulmonary edema
↑ pulmonary vascular resistance
Right ventricular failure
CM- external & nocturnal dyspnea, blood-tinged sputum, cough, cyanosis, fatigue

Right Sided HF

most common cause is left side HF , in the absence of LHF, it is caused by COPD, cystic fibrosis, ARDS
↑ pulmonary vascular resistance
↓ right ventricular emptying
↑ volume & pressure in right ventricle, atrium & great veins
↑ volume in systemic venous circulation
↑ capillary pressure resulting in peripheral edema

Question 32

Factors that increase or decrease peripheral resistance and cardiac output (see chart)

Answer 32

a.) Blood Volume: the higher the blood volume, the greater the amount of work is needed for the heart to pump blood through the circulatory system; ↑Blood Volume = ↑Blood Pressure
b.) Overall Compliance: the elastic characteristics of the vessels contribute to the overall pressure in the vessels; the more elastic the blood vessels are, the lower the blood pressure is; ↑Blood Vessel Elasticity=↓Blood Pressure
c.) Cardiac Output(CO): this is related to heart rate and stroke volume; ↑H.R. and Stroke Volume= ↑C.O= ↑B.P.
d.) Peripheral Resistance: the resistance of the arteries is related to the overall compliance characteristic; ↑Peripheral Resistance = ↓Overall Compliance = ↑Arterial Blood Pressure

Question 33

Classification of blood pressure (see table)

Answer 33

Classification of blood pressure (see table)

WNL <120 mmgHg and < 80 mmHg

Pre-HTN 120-129 or. <80

Stage 1 HTN 130-139 or. 80-89

Stage 2 HTN >140 or. > 90

Question 34

Risk factors for hypertension

Answer 34

Primary HTN
Upper body obesity, family history , advancing age,
sleep apnea, black race, high sodium intake,
low intake of K+, Ca++, Mg++, smoking, alcohol
Pregnancy, Diabetes, psychological stress, dylipidemia

Secondary HTN
Renal disease : renal artery stenosis, renal failure
Adrenal disease : cushing syndrome, pheochromocytoma
Thyroid disease

Question 35

Role of the renin-angiotensin-aldosterone system in hypertension

Answer 35

Modulates vascular tone, influences salt & water retention by kidneys

Question 36

Compare the etiology and pathophysiology of the following types of shock:

Answer 36

Cardiogenic:

-Decreased CO
-Tissue hypoxia
-Adequate -intravascular volume
-Associated w MI, HF, dysrhythmias, acute valvular dysfunction, massive PE

Hypovolemic:

-Loss of whole blood(hemorrhage), loss of plasma(burns),
-Interstitial fluid (DM, DI, emesis, diarrhea, sweating)
-Intravascular volume decreased by 15%

Neurogenic:

Massive vasodilation(decreased SVR)- parasympathetic overstimulation, sympathetic under stimulation
- trauma to spinal cord/medulla
-interruption of O2 supply/glucose to medulla
-bradycardia

Anaphylactic:

Hypersensitivity reaction
-vasodilation, relative hypovolemia, decreased tissue perfusion, impaired cellular metabolism

Septic:
Infection>bacteremia>SIRS
Ends with multiple organ dysfunction syndrome.

Most common sources of infection are: lungs, Urinary tract, GI, wounds, indwelling vascular catheters

Question 37

Pulmonary Alterations

Know the normal values for PO2 and PCO2

Answer 37

The normal values for PCO2 is 35-45, and for PO2 it’s between 80-100mmHg

Question 38

Definition of: hypoxemia, hypercapnia, hypoventilation, hyperventilation, dyspnea

Answer 38

Hypoxemia
↓ PaO2 (oxygenated arterial blood)
Caused by _ decrease oxygen content (high alt.), hypoventilation (COPD), diffusion abnormalities (edema), abnormal ventilation perfusion ration(asthma), pulmonary shunt (RDS)

Hypercapnia
- ↑ CO2, hypoventilation, results in acid base imbalance dysrhythmia, high level results in coma
Caused by : decreased drive to breathe, inadequate ability to respond to ventilatory stimulation

Hypoventilation
- inadequate aveolar ventilation due to pulmonary mechanics or neuro control.
-CO2 removal unable to keep pace with CO2 prod. (hypercapnia)

Hyperventilation
-alveolar ventilation that exceeds metabolic demands, hypocapnia
-occurs with anxiety, acute head injury, conditions that cause insufficient oxygenation of blood

Dyspnea
unable to get enough air
Associated with disturbances of: ventilation, gas exchange, ventilation-perfusion, increased WOB, lung diseases

Question 39

Description of the different types of pneumothorax

Answer 39

Presence of air in pleural space caused by rupture in visceral pleura/parietal pleura. Neg, pressure destroyed
Open-
Tension (life threatening) – associated with decreased venous return & CO (hypoxemia, dyspnea, hypotension)
Spontaneous & Secondary – pain, tachypnea, mild dyspnea

Question 40

Pathophysiology of ARDS

Answer 40

ARDS can be described as acute lung inflammation with alveolocapillary injury; the steps in the causes are..
(1)Decreased surfactant(which impairs the compliance of the lungs)

(2)Endothelial Damage(which increases alveolocapillary membrane permeability, which will lead to pulmonary edema

(3)Vasoconstriction(ventilation-perfusion mismatching)
***THE ROLE OF NEUTROPHILS IS CENTRAL TO THE DEVELOPMENT OF ARDS, because they release many inflammatory mediators like Cytokines, and these mediators can then damage the alveolocapillary membranes, which will increase membrane permeability. These mediators can also cause vasoconstriction.

Question 41

Compare the pathophysiology of the causes of COPD (asthma, chronic bronchitis, emphysema)

Answer 41

All 3 of these Chronic Obstructive Pulmonary diseases are characterized by difficult expiration that results in increased force required to expire, and slowed emptying of the lungs. Asthma and Chronic Bronchitis are similar in that they involve impaired ciliary function, excess mucus production, and bronchospasms. Emphysema differs from them both, because it’s NOT due to any excess mucus, there’s no bronchospasms involved, nor impaired ciliary function. Instead, it involves changes to lung tissues which leads to reduced air flow, which then causes difficulty breathing, and then a reduction in elastic recoil..
Asthma is caused by …
o a hyperactive immune response to an inhaled allergen that will end up activating Eosinophils, B-cells that prod. IgE antibodies that will crosslink onto IgE receptors of Mast cells in the airway and the Mast cells will release mediators
o There’s then, an immediate phase where mast cell-released mediators open up tight junctions, allowing antigens to enter mucosa and activate mucosal mast cells and Eosinophils that will end up releasing more mediators. When this happens, this can cause either 1 of 3 things→ (1)Bronchospasm (2)Inc. Vascular Permeability, which will allow for more cells to come in and release additional mediators(ex: neutrophils, eosinophils, basophils, etc) (3)Increase in mucous production
oThere’s a Late phase where recruited leukocytes release more mediators, there’s factors(esp. from Eosinophils) that cause damage to the epithelium and further mucus production.
*Eosinophils play a key role by slowing ciliary beating, disrupting mucosal integrity, and causing epithelial damage.

Chronic Bronchitis is caused by…
o Inflammation of the Bronchi due to irritants such as smoke, air pollution, etc
oBronchial swelling occurs, there’s excess mucus production, a chronic productive cough, bronchospasm, impaired ciliary function

Emphysema is caused by…
oAbnormal permanent enlargement of airways and the destruction of alveolar walls
oObstruction is from changes in lung tissues, and NOT because of mucous production and inflammation
oMajor mechanism is decreased air flow due to loss of elastic recoil from difficult expiration and hyperinflation

Question 42

Pathophysiology of pulmonary edema, pulmonary embolism, and pulmonary hypertension

Answer 42

Pulmonary Edema: when there’s excess water in the lungs; due to lack of lymphatic drainage, lack of balance between capillary hydrostatic and capillary oncotic pressure, and a lack of capillary permeability.

Pulmonary Embolism: this is an occlusion of a portion of the pulmonary vascular bed by an embolus(most common is a thrombi that’s been dislodged from deep veins in the calf); risk is higher for those who have disorders that promote blood clotting, frequent complication of hospitalization.

Pulmonary Hypertension: The cause for PRIMARY pulmonary HTN is unknown, but in Secondary form of pulmonary HTN causes can be→ COPD, interstitial lung diseases, congenital or acquired heart diseases(ex: mitral stenosis, L Heart failure), or recurrent pulmonary emboli

Question 43

Renal System Alterations

Urine analysis: pH range, specific gravity, protein, blood, glucose, ketones, nitrite, leukocyte esterase, urine microscopy including what the different casts indicate.

Answer 43

The pH: ranges from 4.5-8 usually, and it may indicate whether or not there is a urinary tract or a kidney infection

Specific Gravity: tells you how dilute the urine is/the urine concentration; if it’s not dilute that usually means that you’re not drinking enough fluids.

Protein: can indicate Glomerular disease; trace to 4+ and detects albumin levels; the larger the amount of protein you have the more it may indicate a kidney issue.

Blood: may detect myoglobin and also Glucose; may be a sign of renal damage, kidney stones, infection, cancer; RBCs in blood show sign of kidney disease, blood disorder, underlying condition like a blood disorder

Glucose: sugar doesn’t usually show up in your urine, so if it does that means you’re at risk for Diabetes.

Ketones: are a sign of diabetes

Nitrite: bacteria that can convert nitrate into nitrite; may indicate that there is a U.T.I present

Leukocyte Esterase:detects the presence of WBCs; might be a sign of infection

Urine Microscopy: In urine microscopy, cells are reported as a number per high-power field; there are usually casts involved in urine microscopy and casts are tube-shaped proteins that usually indicate kidney disorders and crystals indicate kidney stones; in the casts you can see RBCs, WBCs, bacteria & yeast, and crystals; the types of casts are usually Hyaline, Granular, Waxy, RBC, and WBC

oHyaline= has Tamm-Horsfall(a protein produced by renal tubular cells of Kidney); one of the most abundant proteins; the development of hyaline casts often suggests a diminished or slow urine flow, which might be a result of excessive exercise, use of diuretic drugs, fever, or acute vomiting; could indicate kidney damage or dysfunction

oGranular= usually pathologic; indicate Acute Tubular Necrosis
oWaxy= broad, formed in tubules of kidneys that have become dilated and atrophic because of chronic disease; waxy casts are non-specific and can be observed in a wide variety of acute and chronic kidney diseases. However, they indicate a certain degree of slowing in urine formation and, therefore, possibly more advanced kidney disease.

oRBCs= if there’s more than 2-3 per High Power Field(HPF), then it’s considered pathologic; a sign of Glomerulonephritis
WBCs= seen in Pyelonephritis (sudden and severe inflammation of kidney due to bacterial infection)

Question 44

Know the major causes and clinical manifestations of prerenal, intrinsic, and postrenal acute renal failure.

Answer 44

Pre-renal: refers to things involving blood flow TO the kidney; you get reduced perfusion due to inadequate blood volume and C.O. along with significant vasodilation; can be due to G.I. losses(ex: vomiting, G.I suctioning, diarrhea, G.I. bleeding); can be due to renal losses(ex: Na+/H2O imbalances from diarrhea, osmotic diuresis, D.M); can be due to skin/resp. losses(ex: burns); movement of fluid into interstitial tissue; crush injuries, acute pancreatitis, internal hemorrhaging.

Intrinsic: involving issues within the kidney itself; most common problem with kidneys(makes up 65% of renal failures)
o Can have Acute Tubular Necrosis(ATN) which is caused by ischemia after it being in a prolonged prerenal state or Nephrotoxicity(from drugs or pigments); Acute tubular Necrosis leads to tubular damage in Proximal Tubule or ascending limb of Henle and is usually irreversible; Clinical Manifestations: oliguric(dec. urine output) or non-oliguric, presence of granular casts on urinalysis
oCan have Acute Interstitial Nephritis(AIN) which is an inflammation of interstitial tissue accompanied by tubular dystrophy; typically see edema of interstitial tissue, infiltration of lymphocytes, or tubular cell damage(in chronic interstitial nephritis you get fibrosis and atrophy of the tubulointerstitial tissue)
oCan have Renovascular disease which is often due to renal infarction/red. blood supply, renal vein thrombosis(blood clot), renal artery occlusion; must be bilateral to cause renal failure

Postrenal: describes flow FROM/OUT of the kidneys; makes up the lowest % of renal failure; obstruction most involve both kidneys to cause renal failure; caused by Benign Prostatic Hypertrophy(BPH), tumor, kidney stones, papillary necrosis, clots, or uteral/pelvic tumor; elevated pressures in your vessels results in adaptive dilation; if obstruction isn’t relieved it can cause nephron destruction or scarring

Question 45

Risk factors for kidney stones.

Answer 45

risk factors for Kidney Stones are: (1)Crystalloid Concentration(↑Ca+, ↑Oxalate, ↓Urine volume); (2)Promoters(↑Uric Acid production, and pH) (3)Inhibitor deficiencies(↓Citrate, ↓Mg) (4)Infections (urease splitting organisms) (5)Anatomical anomalies

Question 46

Most common cause of acute tubular necrosis.

Answer 46

The most common cause of Acute Tubular Necrosis is Ischemia(usually occurs after a prolonged prerenal state)

Question 47

Most common cause of chronic kidney disease.

Answer 47

Number one indicator of the progression of Chronic Kidney Disease(CKD) is Proteinuria; the most common complication of CKD is Hypertension.

Question 48

Risk factors for progression of chronic .” disease.

Answer 48

The risk factors for the progression of CKD is Proteinuria, HTN, Tubulointerstitial fibrosis on biopsy, Hyperlipidemia, smoking, Analgesic abuse, and Ethnicity

Question 49

Definition of chronic kidney disease.

Answer 49

Chronic Kidney DIsease(CKD): the presence of kidney damage or decreased blood level of kidney function for at least 3 months.

Question 50

Following complications of CKD:

Answer 50

Hypertension: if there’s decreased excretion of Na+ and H2O it can lead to HTN and it can contribute to dev. of Chronic Heart Failure(CHF).

-Hyperkalemia : kidneys lose ability to secrete K+; decrease K+ intake so it doesn’t build

-Renal osteodystrophy: decreased production of Vitamin D; decreased gut absorption of Ca+; Hypocalcemia; retention of “toxic” metabolites(ex:Osteomalacia, impaired bone growth in children)

Question 51

Blood and Blood disorders

Regulation of erythropoiesis

Answer 51

Erythropoiesis is basically regulated w/ the hormone Erythropoietin in a negative feedback loop. Basically, when the blood O2 levels begin to decrease, the Kidney cells will detect this drop. In response, the kidney cells will signal the kidney to increase its production of EPO and release it into the blood. This then increased bone marrow and then, now, we get increased RBC production. Overall, tissue hypoxia in the kidneys causes erythropoietin release that stimulates proliferation of erythrocytes.

Question 52

Definition of the following terms: microcytic, macrocytic, hypo/hyperchromic, anisocytosis, poikilocytosis

Answer 52

Microcytic: unusually small RBCs; Macrocytic: unusually large RBCs; Hypochromic: decrease in HgB concentration, so there’s not enough pigment that carries O2; Hyperchromic: high HgB concentrations, so there’s too much pigment that carries O2; Anisocytosis: RBCs that are of unequal size; Poikilocytosis: RBCs in varying shapes(i.e. sickle shape, oval, teardrop)

Question 53

Role of platelets

Answer 53

They help to constrict damaged blood vessels, form hemostatic plugs in injured blood vessels(blood clots), provide substances that accelerate blood clotting(factors III, Factors XIII).

Question 54

Pathophysiology and clinical manifestations of: aplastic anemia, pernicious anemia, folate deficiency anemia, hemolytic anemia, iron deficiency anemia, thrombocytopenia (idiopathic, thrombotic), thrombocythemia, DIC

Answer 54

Aplastic Anemia:is a red. in RBCs, WBCs, and platelets from bone marrow suppression; Clinical Manifestations are usually: S.O.B, rapid H.R, headache, fever, tiredness; can be autoimmune disorders directed at blood stem cells; can be idiopathic or from total body radiation, can be familial, or from infections(ex: HIV, Hepatitis)

Pernicious Anemia: there’s a slow onset, but by the time of diagnosis symptoms are severe; characterized by B12 deficiency(usually cause of gastritis or absence of intrinsic factor needed to absorb B12 or can be cause of genetics); Clinical Manifestations are usually: weakness, fatigue, paresthesias, ataxia, sore throat, red tongue, low HgB, high Hematocrit, High MCV, low B12.

Folate Deficiency Anemia: Characterized by a deficiency in Folate which is essential for DNA and RNA synthesis; Pathophysiology is low serum folate; Clinical Manifestations are: similar to pernicious anemia, severe chelosis(swollen red patches at mouth corners), and stomatitis(inflamed and sore mouth)

Hemolytic Anemia: Hemolysis/destruction of RBCs by way of the immune response(ex: transfusion rxn), trauma(ex; prosthetic heart valve, blood clot disorder), infection(ex: bacterial, viral), drugs,/chemicals, physical(ex: burns, radiation)or via genetics(ex: sickle cell anemia); Hematocrit and Hemoglobin levels are low and there’s a low amount of reticulocytes(immature RBCs); Clinical Manifestations are typically: hemolysis, reticulocytosis, anemia, aplastic crisis(sudden cessation of bone marrow activity), infection(loss of splenic function), pain episodes, hand-foot syndrome(swelling of hands and feet), stroke, acute chest syndrome(dyspnea, chest pain, fever, vision problems, delayed growth, inc. risk for preterm and low weight babies)

Iron Deficiency Anemia: deficient iron intake or when the demand for iron exceeds the supply of it(usually due to deficient iron intake, blood loss via G.I. bleed, metabolic iron deficiency, insufficient delivery of iron to bone marrow); Pathophysiology is: Stage 1(body iron stores depleted), Stage 2(iron transport to bone marrow is diminished; iron deficient erythropoiesis); Stage 3(small HgB deficient cells enter the circulations resulting in manifestations); Clinical Manifestations are: weakness, fatigue, S.O.B, paleness, more advanced clinical manifestations(ex: brittle nails, tongue abnormalities, stomatitis/mouth swelling, dysphagia/difficulty swallowing, neurologic conditions).

Idiopathic Thrombocytopenia: in general Thrombocytopenia is when platelet count is below 150,000;
oAcute idiopathic occurs more frequently in children and lasts 1-2 months, and it’s usually 2ndary to an infection(usually viral); Pathophysiology is that it occurs w/o Lupus and is assoc. w/ an inc. in antigens in the blood and the antigens form a complex w/ circulating antibodies
oChronic Idiopathic is most common in women between 20 & 40 and is progressive; Pathophysiology is that Ig antibodies are directed to platelet glycoproteins and antibody-coated platelets are then recognized and removed by macrophages in the spleen
-Clinical Manifestations for both Acute and Chronic Idiopathic are petechiae and purpura which may progress to major hemorrhage and cause symptoms like wt. loss, fever, and headaches)
- Thrombotic Thrombocytopenia:an occlusion of arterioles and capillaries by aggregated platelets; Pathophysiology is platelet depletion, organ ischemia, assoc. w/ dysfunction of the plasma metalloprase ADAMTS14(enzyme responsible for cutting willebrand factor into smaller molecules and defects in this enzyme cause large molecular wt. von willebrand factor on cell surface–which results in aggregates of platelets which can form vessel occlusions)
-Clinical Manifestations: severe thrombocytopenia(<20,000), hemolytic anemia, ischemia(which most likely involves CNS side effects), kidney failure, fever, and you’ll see an inc. in LDL and LDH.

• Thrombocythemia: when the platelet count exceeds >600,000
  oEssential(Primary): thrombopoietin levels are increased
  oSecondary: Splenectomy(spleen doesn’t remove platelets from circulation) or inflammatory conditions(excessive prod. of cytokines causes an inc.in thrombopoietin)
• The Clinical Manifestations for Thrombocythemia are: arterial or venous thrombosis, ischemia, nervous system may be involved(headache, dizziness, paresthesias, stroke, visual disturbances), myocardial and renal arteries may be involved

D.I.C: an acquired clinical syndrome involving widespread activation of clotting; you get multiple clots that disrupt blood flow to the organs–resulting in multi-organ failure; clotting results in consumption of platelets and platelet clotting factors leading to severe bleeding.
oStep 1 of D.I.C→ endothelial injury, tissue injury, inflammation
oStep 2 of D.I.C→ release of large amounts of tissue factor
oStep 3 of D.I.C→ Tissue Factor initiates clotting cascade leading to production of thrombus, which leads to the production of Fibrin, which leads to the formation of a fibrin clot.
-there’s platelet activation that leads to a microvascular thrombosus, ischemia, necrosis. Then, these things can cause impaired organ perfusion leading to end organ failure. The kinin system gets activated, followed by activation of the complement system, which leads to increased permeability of vessels, and then Hypotension and shock can soon follow
oStep 4 of D.I.C→ factors like Tissue Necrosis Factor induce inhibitors that prevent the synthesis of Plasma, so you get diminished Fibrinolysis ability and, therefore, can’t destroy fibrin
oStep 5 of D.I.C→ these fibrin products trigger cytokine release from monocytes, and this can result in further damage to the endothelium and cause further Tissue Factor release.
oStep 6 of D.I.C→ consumption of platelets and clotting factors leads to hemorrhage.
Clinical Manifestions of D.I.C: bacterial, viral, or parasitic infections, tissue damage, inflammation, neoplastic disorders, C.V. disorders, fat embolism, liver cirrhosis, P.E, hypothermia, placental abruption

Question 55

Pathophysiology of sickle cell anemia (including genetic alteration)

Answer 55

Sickle cell anemia is caused by a glutamine to valine substitution; genetics can cause a mutation of HBB gene(which codes for B-Hemoglobin), and the mutation of that gene ends up calling for the nucleotide change from Thymine to Adenine; you get inflammation which causes abnormal erythrocyte membrane and the presence of chronic hemolysis which ends up triggering an inflammatory response and endothelial dysfunction.
HbAs= sickle cell trait; HBSS=sickle cell disease; HbAA=normal child/adult
Lost of splenic function usually because of infection is associated with sickle cell anemia, and pain is the most common symptom of sickle cell anemia/disease; can get aplastic crisis(sudden cessation of bone marrow activity), hand-foot syndrome(swelling of hands-feet), stroke, vision problems, delayed growth,

Question 56

Endocrine Disorders
Definition of negative feedback (be able to give an example i.e. regulation of thyroid hormone)

Answer 56

Negative feedback works to restore homeostasis by correcting the disruption in it. In the case of hormones, it helps to keep the thyroid hormone within its normal range.

Question 57

Clinical manifestations, pathophysiology, and diagnosis of hypothyroidism and hyperthyroidism

Answer 57

Hypothyroidism: associated with the impairment of thyroid hormone output that leads to a hypometabolic state; some of the most common causes of Hypothyroidism are→ Hashimoto’s disease(blocks autoantibodies to the TSH receptor), large resection of the thyroid gland, radioactive iodine therapy, iodine deficiency; The clinical manifestations in children/during fetal dev.is cretinism(retardation of physical and intellectual growth as well as impaired skeletal growth/brain development), in adults it’s myxedema(slowed mental and physical activity; initial symptoms are fatigue, lethargy, cold intolerance, apathy; sleep apnea may develop; peripheral edema cause of accumulation of mucopolysaccharides); DIagnosed by having increased TSH levels, and lowered T4, and presence of antithyroid peroxidase antibodies in the serum(usually if they have Hashimoto’s Disease)

Hyperthyroidism: Primary causes of hyperthyroidism are→ Grave’s Disease, hyperfunctional multinodular goiter, hyperfunctional adenoma/benign tumor, thyroiditis(inflammation of thyroid that causes inc. in thyroid release), thyroid cancer; Secondary causes of Hyperthyroidism are→ TSH-secreting pituitary adenoma; common clinical presentations of thyroid disease are: palpitations, fatigue, wt. loss, tremors, excessive sweating, and heat intolerance. Typically cardiac symptoms are an early hallmark of hyperthyroidism
o Graves’ Disease: an autoimmune disease initiated by igG antibodies against specific domains of the TSH receptor(TSH binds to receptor and stimulates inc. release of thyroid hormones and the TSH stimulates more cells and more cells=more thyroid); you get hyperfunctioning diffuse hyperplastic goiter A.K.A overworked, spread out over a large area, enlarged goiter, ophthalmopathy(enlarged eyes), dermopathy(late characteristic where you have specks/pittings of edema); since Graves disease is an autoimmune disorder, the actions of these igG antibodies can’t be regulated by negative feedback of thyroid hormone; Diagnosed by labs showing→ decreased TSH levels, elevated T3 and T4

Question 58

Major actions of the following hormones in the regulation of glucose homeostasis: insulin, glucagon

Answer 58

Insulin and glucagon are hormones that work together to maintain glucose homeostasis in the body. Insulin is secreted by the pancreas in response to elevated blood glucose(usually following a meal). Insulin lowers blood glucose by increasing glucose uptake in muscle and adipose tissue and by promoting glycolysis and glycogenesis in liver and muscle. Glucagon, on the other hand, is secreted by the pancreas when blood glucose levels drop. Glucagon raises blood glucose levels by stimulating glycogenolysis (breakdown of glycogen) and gluconeogenesis (synthesis of glucose from non-carbohydrate sources) in the liver.

Question 59

Compare the pathogenesis of Type I and Type II diabetes

Answer 59

Type 1 (IDDM)

-lack of insulin due to reduced B-cell mass from genetic susceptibility, autoimmunity, & environmental factors.
Non/immune
CM- hyperglycemia, glycosuria, polyuria ,polydipsia , polyphagia ,weight loss, ketoacidosis, diabetic coma

Type 2 (NIDDM)

-nonspecific symptoms of fatigue, pruritus, recurrent infections, visual changes, paresthesia
Increased risk of cardiovascular disease
Causes – obesity & sedentary lifestyle
Insulin resistance: ↓number of insulin receptors, impaired signaling, decrease synthesis and/or translocation of GLUT-4 in muscle & fat cells.
- Increase in hepatic gluconeogenesis
Insulin deficiency: hyperglycemia —>reduced insulin secretion-decreased GLUT-2 transporter, absence of oscillations of insulin secretion

Question 60

Therapeutic goals for a patient with diabetes (e.g. fasting blood sugar, hemoglobin A1C, LDL, HDL)

Answer 60

a.) Fasting Blood Sugar→ <110 mg/dL c.)LDL→ <100
b.) Hemoglobin A1c→ <5.7% d.) HDL→ >45 for men and >55 for women

Question 61

Pathophysiology and clinical manifestations of Cushing disease/syndrome and Addison’s disease

Answer 61

Cushing’s Disease/Syndrome: elevated cortisol (hypercortisolism). majority have a pituitary adenoma/benign tumor which secretes excess ACTH, loss of normal feedback inhibition by cortisol (i.e. the ACTH secreted by the tumor is not regulated by increased cortisol levels); most common cause of Cushing’s Syndrome is prolonged use of glucocorticoids; other cause include→ 1) ectopic ACTH-secreting tumors 2) Cortical-secreting adrenal tumors

oClinical Manifestations of Cushing’s Disease→ Weight gain is the most common feature and often the initial symptom – related to accumulation of adipose tissue in the trunk, facial, and cervical areas (i.e. moon face, buffalo hump). Other manifestations include…

1. Glucose intolerance due to cortisol-induced insulin resistance, increased gluconeogenesis and increased glycogen storage. Cortisol antagonizes the action of insulin in peripheral tissues.
2. Muscle wasting, specifically in the muscle of the extremities, due to excess protein catabolism and decreased muscle protein synthesis (causes muscle weakness).
3. Increased bone resorption, inhibits bone formation, decreases intestinal calcium absorption, and increases renal calcium excretion – osteoporosis and fractures.
4. Hypercalciuria and renal stone formation
5. Glucocorticoid excess inhibits fibroblasts, leading to loss of collagen and connective tissue. Thinning of the skin, abdominal striae, easy bruisability, poor wound healing, and frequent skin infections.
6. Hyperpigmentation – associated with high levels of ACTH (results in a bronze color)
7. Hypertension (75-85%) – increased vascular sensitivity to catecholamines leading to vasoconstriction and hypertension.
8. Suppression of the immune system – increased susceptibility to infections, especially fungal infections (poor wound healing).
9. Alterations in mental status (irritability and depression to severe psychiatric disturbances).
10. Females – increased hair growth, acne, and oligomenorrhea due to increased adrenal androgen levels.
11. Men – decreased testosterone secretion – decreased libido, loss of body hair, and impotence.
    - Addison’s Disease: a decrease in the Aldosterone secretion from the Adrenal glands; there are idiopathic and secondary pathophysiology for Addison’s disease;

o If it’s Idiopathic it’s usually the result of an autoimmune disease where there’s antibodies specifically targeting cells of the Adrenal Cortex, there’s a defect in immune surveillance mechanisms and so there becomes a deficiency in immune-suppressor cells.There can also be atrophy of the cortex

o If it’s Secondary, there’s low to absent ACTH levels which leads to a decrease in cortisol secretions from the adrenal cortex.( In this type of hypocortisolism, aldosterone levels are normal); there’s inadequate adrenal stimulation, adrenal atrophy occurs, then dec. in the synthesis of corticosteroids; Usually what triggers secondary development of Addison’s Disease is (1)exogenous administration of glucocorticoids (2)surgical removal of ACTH/cortisol-secreting hormone (3)pituitary hypofunction (4)pituitary removal (5)ACTH deficiency

oClinical Manifestations of Addison’s Disease: Symptoms usually begin gradually. Some common ones are→ (1)weakness (2)fatigue (3)anorexia (4)wt. loss (5)nausea (6)diarrhea (7)orthostatic hypotension (8)hyperpigmentation (8)Females – loss of pubic and axillary hair (due to decreased adrenal hormones)

Question 62

Musculoskeletal Pathophysiology

Common musculoskeletal conditions by age group

Answer 62

Children: trauma, congenital defects, sequelae of chronic illness(pathological condition resulting from a prior disease, injury, or attack)
Adolescents: growth delay, epiphyseal injuries, bone lesions
Adults: imbalance of bone modeling, trauma, repetitive stress, cumulative load (important mechanism contributing to musculoskeletal injury and pathology), pregnancy
Mature Adults: bone loss, joint degeneration, neurological/sensory changes, falls, drug therapy

Question 63

Compare osteoblasts, osteoclasts, and osteocytes

Answer 63

Osteoblasts: bone formation
: assists w calcification, help concentrate nutrients in the matrix
Osteoclasts: bone resorption

Question 64

Describe the process of bone remodeling

Answer 64

• The purpose of bone remodeling is to replace old bone tissue w/ new bone tissue and is a type of preventative maintenance process. Typically it takes about 3-4 months.
• Stage 1(Resting Phase): period of rest during bone formation
• Stage 2(Activation): pre-osteoclasts are attracted to remodeling sites
• Stage 3(Resorption): osteoclasts dig out a cavity
• Stage 4(Reversal): mononuclear cells appear on the bone surface
• Stage 5(Formation): osteoblasts lay down new bone til’ resorbed bone is completely replaced.

Question 65

Know the components of a synovial joint

Answer 65

• Synovial joints are made up of five classes of tissues. These include bone, cartilage, synovium, synovial fluid, and tensile tissues composed of tendons and ligaments.
• The synovial joint is also called the “diarthrodial joint” and is formed by three basic components: the joint cavity, the joint(articular) cartilage, and the joint capsule.
• oJoint cavity- Synovial fluid is a viscous fluid that fills the synovial cavity and acts as a lubricant for smooth movement of bone
• oJoint(Articular) Cartilage- covers the surfaces of articulating bones; the smooth and slippery lubricated surface of the articular cartilage is what covers the ends of bones, allowing the sliding of bones at the joint without rubbing each other
• oJoint Capsule- is composed of a synovial membrane layer lining up the joint cavity and a fibrous layer(the fibrous connective tissues are what help to connect muscles to bones) and it surrounds the joint;

Question 66

List the steps in the healing of a fracture

Answer 66

• Step 1: a fracture occurs/there’s a disruption to the periosteum and blood vessels
• Step 2: there’s bleeding at the site, which leads to the inflammatory response and eventual clot formation
• Step 3: necrosis starts to happen along the fracture line
• Step 4: there’s the activation of bone-forming cells
• Step 5: Osteoblasts start to synthesize collagen and bone matrix, and then bone remodeling eventually occurs
• The healing of a fracture can be divided into three phases: inflammatory phase, reparative phase, and remodeling phase. The inflammatory phase is the first stage of healing and begins immediately upon fracture. A blood clot forms allowing the influx of inflammatory cells to the wound area. This is followed by a cytokine cascade that brings repair cells into the fracture gap. The reparative phase begins with the formation of a soft callus made up of fibroblasts and chondroblasts. The soft callus then hardens into a hard callus made up of osteoblasts and chondroblasts. The remodeling phase involves the replacement of woven bone with compact bone

Question 67

Pathophysiology and clinical manifestations of the following:

Answer 67

Osteoporosis: increased loss of bone mass
-imbalance between bone resorption & formation
-menopausal changes
-calcium deficiency
-vertebral fractures most common, complications -pulmonary embolism, pneumonia
Risk- age, lack of physical, inadequate calcium & vitamin d, excessive alcohol, smoking

-Sprains/strains
-Rhabdomyolysis: Rhabdomyolysis: a complication of severe muscle trauma
oPathophysiology→ traumatic crushing of muscle, obstruction of blood supply to muscle, excessive muscle strain or activity, thermal injury, electrical
oClinical Manifestations→ principle manifestation is myoglobinuria(dark urine), large levels of muscle enzymes in serum, pain and tenderness of affected muscle, serum electrolyte alterations(ex: large levels of K+/Hyperkalemia); complications can be renal failure, tachycardia, cardiac dysrhythmias, metabolic and respiratory acidosis, temperature elevation

-Osteoarthritis : inflammation of synovial joints: loss & damage of articular cartilage, thickening of joint capsule, subchondral bone changes
-effects primarily load bearing areas
CM-pain (may be referred), stiffness, swelling, limited ROM

-Rheumatoid arthritis : A systemic autoimmune diseases that causes chronic inflammation in multiple joint; synovial membrane is usually the first to be effected
oPathophysiology→ an antigen activates CD4 helper T-cells and most likely b-cells; the T-cells express RANKL–which wlll promote osteoclast formation and lead to bony erosion; inflammatory cytokines induce enzymatic breakdown of cartilage and bone
oClinical Manifestations→ gradual onset, fever, fatigue(systemic manifestations of inflammation), joints become painful and tender and stiff, joint swelling, loss of R.O.M, joint deformity, rheumatoid nodules, systemic symptoms

-Gout: a byproduct of protein metabolism that normally assists with removal of nitrogen waste from the body; at low levels it’s an antioxidant, but at high levels it’s a pro-oxidant and causes inflammatory changes
oPathophysiology→ inflammatory response to uric acid production, resulting in high levels of uric acid in the blood and other body fluids; uric acid concentration exceeds 6.8mg/dL and ends up crystallizing and forms insoluble complexes of urate that deposit in connective tissue; crystallization happens in synovial fluid which triggers an inflammatory response by macrophages; these macrophages then phagocytize urate crystals–forming an inflammasome(protein complex that regulates immunity); inflammasomes convert inactive interleukins into their active form–prolonged accumulation results in joint damage; Urate crystals trigger the acute inflammatory response
oClinical Manifestations→ hyperuricemia(high level of uric acid); recurrent attacks of monoarticular arthritis, MSU deposits in and around the joints; renal disease/uric acid stones
The clinical stages are.. (1)Asymptomatic hyperuricemia (2)Acute gouty arthritis (3)Tophaceous gout(severe gout)

Question 68

Nervous System Disorders
Sympathetic vs. parasympathetic nervous systems (very brief review)

Question 69

Fundamentals of an action potential (e.g. depolarization, repolarization, threshold, resting potential

Question 70

Compare the pathophysiology and clinical manifestation for the following disorders:
Alzheimer’s disease (both early onset and late onset)

Parkinson’s disease
Amyotrophic Lateral Sclerosis
Myasthenia Gravis
Multiple Sclerosis

Question 71

Compare the etiology and pathophysiology of ischemic (thrombotic and embolic) and hemorrhagic stroke (including transient ischemic attack)

Answer 71

Thrombotic stroke: arterial occlusions caused by thrombi in the arteries supplying the brain/intracranial vessels
- Development linked to atherosclerosis,arthritis, increased coagulation, dehydration ,hypotension, prolonged vasoconstriction
Embolic stroke: involves fragments that break away from a thrombus formed outside
the brain(heart, aorta, carotid, thorax); involves small vessels & obstructs at a bifurcation/other point of narrowing
- Atrial fibrillation major conditions associated , others include MI, endocarditis, rheumatic heart disease
Hemorrhagic stroke : intracranial hemorrhage
- HTN, ruptured aneurysms, arteriovenous malformations, bleeding into tumor
Transient ischemic attacks: focal ischemic cerebral neurologic deficits brain angina), deficit lasting <1hr, causes are same as ischemic stroke. Warning of impending stroke

Question 72

Know the differences between generalized and partial seizures

Answer 72

Generalized seizures
- Involve neurons bilaterally , often no local onset, usually originate from subcortical/deep brain focus
- Consciousness is always impaired/lost
- Tonic, clonic, myoclonic
Focal seizures
- Involve neurons unilaterally, often have a local onset and usually originate from cortical brain tissue
- LOC may/may not occur, may become Geraldine’s and lasts <2mins – simple or complex

Question 73

Know the pathophysiology of seizures (e.g. alterations in the resting membrane potential)

Answer 73

Sudden change in membrane potential of a group of neurons: defect in GABA, channel abnormalities, abnormalities in excitatory transmission
-if uninvited, excitation neurons spread to contra lateral cortex and subcortical areas-basal ganglia, thalamus, brain stem
-tonic phase: phase of muscle contraction once spread to subcortical area o brain ,associated w LOC
-clonic phase : phase of alternating contraction & relaxation of muscles, which begins as inhibitory muscles begin to inhibit cortical excitation

Question 74

Pain Pathophysiology
Know the afferent pathway of pain (starting at the receptor).

Question 75

Know the Gate Control theory of pain (small vs. large fibers)

Answer 75

Nociceptor impulses are transmitted by specialized skin receptors ro spinal cord thru A & C fibers
stimulation of large fibers trigger cells to “close gate “, which decreases transmission of impulses, & diminishes pain perception
stimulation of small fibers “ opens the gate”, enhances pain perception

Question 76

Describe the function of supstance P and glutamate in the transmission of pain.

Answer 76

Substance P= activates ascending pathways
Glutamate = AMPA, NMDA

Question 77

Know the different types of pain nociceptors.

Answer 77

Mechanical – cutting, crushing, pinching.
Thermal -temp extremes (esp. heat)
Polymodal- respond to all kinds of damaging stimuli including irritating chemicals released from injured tissues
(all can be senitized by prostaglandins)

Question 78

Describe the role of the efferent nerve fibers in the modulation of pain.

Answer 78

Responsible for inhibition of afferent pain signals ***
Efferent neurons form synapses with structures in medulla that inhibit pain, impulses are transmitted back thru spinal pain to dorsal horn to block transmission of nociceptive impulses

Question 79

Know the difference between first, second, and third order neurons.

Answer 79

1st – A (myelinated fibers
Fast (30 m/sec), occurs on stimulation of mechanical & thermal nociceptors, carry well localized sharp pain sensations
2nd -C fibers (unmyelinated)
Slow (12 m/sec), on stimulation of polymodal nociceptors, diffuse aching/burning sensations, poorly localized
Activated by chemicals like bradykinin & capsaicin
Unpleasant , persists for longer time

Question 80

Know the role of the difference areas in the brain in the perception of pain.
Compare acute and chronic pain.

Question 81

Define the following:

Pain threshold
Perceptual dominance
Pain tolerance
Referred pain
Somatic pain
Psychogenic pain

Answer 81

Pain threshold: the point at which a stimulus is perceived as pain.

Perceptual dominance: intense pain at one location may cause an increase in threshold in another location.

Pain tolerance: duration of time/instensity of pain that an individual will endure before initating overt pain responses. Influenced by – cultural perception, expectations, role, physical & mental health.

Referred pain: present in area distant from its point of origin, supplied by the same spinal segment as actual site of pain

Somatic pain: pain with a cause (MI)

Psychogenic pain : no known physical cause, not imaginary

Question 82

HIV Disease
Describe the HIV life cycle (include the role of the proteins gp120 and gp41)

Question 83

Define CD4 and viral load

Answer 83

CD4
- normal >500
- immunocompetency, predicts progression
Viral load
- measures amount of circulating virus, reflects viral prod in all cells.
- increased in infection & associated w progression.

Question 84

Describe the different stages of HIV/AIDS infection

Answer 84

Initial/early stage
- Immune responds quickly & symptoms disappear in 2 weeks
- HIV antibody test becomes positive w/in 4-6weeks after infection, avg 30 days (seroconversion)
Chronic HIV
- Contrast pattern of viral production-CD4 destruction
- Lasts for several years without symptoms, eventually body’s immune system is developed and individual develops symptoms – lymphadenopathy, skin problems
Advanced stage/AIDS
- Labs indicate severe immunosuppression – CD4 <200 cells
- One or more of 26 AID conditions: opportunistic definitions, neoplasticism disease, neurologic manifestations

Question 85

Describe the manifestations of the opportunistic infection that were discussed in class

Answer 85

Thrush/candida/yeast in mouth, esophagus, vagina
Pneumocystis pneumonia (PCP):
- life threatening if untreated, symptoms of fever, dry cough, SOB, fatigue, weight loss; prophylaxis recommended when CD4 ≤ 200 cells
-Cytomegalovirus (CMV)
- most commonly affects eyes causing retinitis and blindness
Eye symptoms- floating spots in eye, hazy vision, blurred/blind spots
GI- diarrhea, loss of appetite
Mycobacterium Adium Complex (MAC)
- affects lungs & intestines; severe when spread to organs like BM, liver & spleen . Symptoms of weight loss, stomach pain, diarrhea, fever , night sweats, fatigue
-rarely occurs when CD4>100 cells, prophylaxis when CD4<50 cells
Toxoplasmosis-
- caused by parasites that infects CNS from animal feces & uncooked meat.
Symptoms of confusion, seizures, headaches, numbness, coma
Prevention - don’t change cat litter, wear gloves when gardening, & fully cook all meats & eggs

Question 86

GI Pathophysiology
Etiology and pathogenesis of vomiting and constipation.
Clinical manifestations and pathogenesis of the different types of diarrhea (e.g. secretory, osmotic, exudative, deranged motility).

Question 87

Risk factors, pathophysiology, and clinical manifestations of the following:
-GERD:
-Gastritis:
-Peptic ulcer disease:
-Ulcerative colitis:
-Crohn’s disease:

Answer 87

-GERD: · reflux of chyme from stomach to esophagus
Risk- obesity, H. Pylori
Relaxation/weakness of lower esophageal sphincter, increased abdominal pressure, delayed gastric emptying (Ulcers), hiatal hernia
- CM: heartburn, upper abdominal pain w/in 1hr of eating, symptoms worsen when lying down/increase in intra-abdominal pressure
-Gastritis : inflammatory disorder of gastric mucosa lining from drugs (NSAIDS), alcohol, H. Pylori
-Peptic ulcer disease
-Ulcerative colitis
-Crohn’s disease

Question 88

Protective mechanisms of the gastric mucosa
Alterations that cause liver failure
Pathogenesis of Alcohol liver disease
Pathophysiology of cirrhosis
Hepatitis A, B, C, D, E – transmission, acute vs. chronic infection, consequences of infection (know what the different lab values indicate)