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Patho exam study guide, Study notes of Pathophysiology

Patho cumulative final exam study guide

Typology: Study notes

2022/2023

Available from 06/01/2023

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Module Learning Objective Topic
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Module Learning Objective Topic

1 Differentiate between immunocompetence and immunosuppression

  • Immunocompetence : this is the bodyโ€™s ability to produce a normal immune response
  • Immunosuppression : this is when someoneโ€™s immune system is weakened, making it more difficult to fight infections and other diseases Immunodeficien

1/13 Identify key lab values in inflammatory and infectious diseases. โ— CRP: (c-reactive protein) โ—‹ Normal: CRP <1.0 mg/dL โ—‹ Autoimmune disease: 1<CRP< โ—‹ Infection: CRP>10 mg/dL โ—‹ Acute bacterial infection: CRP>50 mg/dL โ— ESR: (erythrocyte sedimentation rate) โ—‹ 0-15 mm/hr in males โ—‹ 0-20 mm/hr in females โ— Fibrinogen โ—‹ Normal: 200 to 400 mg/dL โ— WBCs: โ—‹ Normally 4,000-10, โ— Neutrophils: โ—‹ Normally 40-60% of WBCs โ—‹ Absolute neutrophil count (ANC): 2,500- โ—‹ Neutropenia: <1, โ— PCT > 0.25 ng/mL = infection โ—‹ PCT = procalcitonin โ—‹ Normal <0. Explain pathophysiologic changes in white blood cells. Normal White blood cell range 4,000-10,000 mcL โ— Elevated counts โ—‹ Occur during acute infection โ—‹ Leukemoid reaction leukocytosis from reasons other than leukemia, over 50, โ— Reduced counts โ—‹ Occurs if infection has depleted supply or bone marrow is suppressed โ—‹ leukocytes of less than 4, โ— Left shift โ—‹ Name for when higher proportion of neutrophils are immature. Bone marrow releases more immature neutrophils in response to infection. Left shift indicates acute infection. Infection Rev. SPR 23

NUR 376 Final B Blueprint

2 Identify the various body compartments and mechanisms for fluid movement โ— Key concept #1: how could someone be hypervolemic and dehydrated? โ—‹ They could have lots of hypertonic solution in them (hypervolemic) that is pulling water out of their cells (dehydrating them) โ— Key concept #2: What is Starlingโ€™s Law of capillary forces? โ—‹ Hydrostatic vs osmotic+oncotic pressures compete at capillary beds โ—‹ Hydrostatic pushes outward, the other two pull the water back in โ— Fluid compartments โ—‹ Intracellular: โ–  40% of adult body weight โ—‹ Extracellular fluid: โ–  20% of adult body weight โ–  80% of ECF is in blood vessels โ—‹ Interstitial: โ–  Between cells or between capillaries โ— Mechanisms for fluid movement โ—‹ Transport mechanisms โ–  Diffusion โ–  Osmosis โ–  Facilitated transport โ–  Active transport โ—‹ Pressures โ–  Osmotic: PULLS H2O towards areas of higher solute concentration โ— PULLS H2O back into capillaries at distal ends of capillary beds. Opposes hydrostatic pressure. โ–  Oncotic: proteins PULL H2O โ— Low serum albumin (like in starvation) leads to lower oncotic pressure, more fluid leaking out of vessels, edema โ–  Hydrostatic: force of blood PUSHing against capillary walls Compare and contrast isotonic and hyper/hypotonic IV solutions, including the effect on fluid shift โ— Isotonic: 0.9% NaCl, LR โ— Hypotonic: 0.45% NaCl, D5W โ— Hypertonic: 3% NaCl Hypervolem cellular dehydration hydrostatic/ osmotic pressures Types of flu

โ—‹ Origin: adrenal gland โ—‹ Site of action: kidneys โ—‹ Effect: Stimulates Na+/H2O retention, K+ excretion by kidneys => increase in BV, BP, Na+; decrease in K+ Explain how the RAAS affects fluid balance. Pg 120 โ€œThe RAAS. When there is a decrease in circulation or drop in blood pressure , the kidney senses decreased perfusion and releases renin. Renin cleaves angiotensinogen, which is a protein produced by the liver, to produce angiotensin I. In the lungs, ACE transforms angiotensin I into angiotensin II. Angiotensin II is a potent arterial vasoconstrictor; it also stimulates the adrenal gland to release aldosterone. Aldosterone increases sodium and water reabsorption into the bloodstream at the nephron. It also causes potassium excretion from the bloodstream into the urine. The net effect of the RAAS is to raise blood volume and increase blood pressure.โ€

2 Distinguish between the four types of acid/base disturbances โ— Respiratory alkalosis โ—‹ Etiology: hyperventilation from anxiety or inappropriate ventilator settings causes person to breath off too much CO โ— Respiratory acidosis โ—‹ Etiology: not breathing off enough CO2, as in COPD or thoracic trauma โ— Metabolic alkalosis โ—‹ Etiology: vomiting out your acid, ingesting bicarbonate, issue with kidney excretion of H+/HCO3- โ—‹ Gain a base or lose an acid โ— Metabolic acidosis โ—‹ Etiology: intense diarrhea causing you to lose a base, issue with kidneys where you donโ€™t excrete enough H+ or excrete too much bicarb, ketoacidosis, diabetic ketoacidosis, buildup of uremic acid โ—‹ Gain an acid or lose a base Normal lab values- โ— Blood pH : 7.35-7. โ— PCO 2 : 35 to 45 mmHg โ— PO 2 : 90-100 mmHg โ— HCO 3 : 22 to 26 mEq โ— SaO 2 : 95-100% Etiology

capillary beds โ—‹ Heart muscle hypertrophy โ—‹ HF โ—‹ MI โ—‹ Hemorrhagic stroke

3a Describe the concept of cardiac output and key symptoms found with dysfunction. CO=SV*HR. Decreased stroke volume โ€“ due to decreased venous return, for example โ€“ results in decreased CO. Decreased CO leads to poor delivery of oxygenated blood to tissues, leading to compromised perfusion, lower BP, compensation by RAAS and nervous system, and potentially increased BP, HR, and strength of heart contraction. โ– ยท Hypotension โ– ยท Hypercapnia โ– ยท Cardiac arrhythmias โ– ยท Chest pain โ– ยท Poor tissue perfusion (diminished pulses) โ– ยท Clammy, cool skin โ– ยท Dizzy/lightheaded/syncope โ– ยท Fatigue โ– ยท Weakness โ– ยท Edema โ– ยท Decreased urine output Deceased C and SV 3a Differentiate between Peripheral Artery Disease and Coronary Artery Disease. โ— PAD most commonly presents in femoral artery โ€“ leg pain, swelling, redness, intermittent claudication โ— CAD is in coronary arteries โ—‹ SOB, MI, angina Clinical Manifestatio

4 Compare and contrast the concepts of ventilation, oxygenation, and perfusion. โ— In relation to orthopnea: โ€œWhen a patient (with heart failure) is in the supine position, the fluid accumulation in the lungs becomes distributed throughout the lung fields. The supine position disperses the fluid within the lungs, which worsens the oxygen diffusion from the alveoli into the pulmonary capillaries.โ€ DA p. 417 โ— In other words: orthopnea occurs because oxygenation is most impaired in the supine position Orthopnea Rev. SPR 23

NUR 376 Final B Blueprint