Final Exam Information

• Final Exam on Friday, April 25th at 10am
• Location: To Be Determined; check announcements next week
• Blank scrap paper will be provided
• Review syllabus and student handbook for exam policies
• If unable to take the exam as scheduled, an incomplete will be needed
• Incompletes need to be resolved before the start of the next semester
• Make-up exams are in-person

Exam Components

• The exam will consist of 60 questions
• 1/3 of the questions will relate to shock
• Another 1/3 of the questions relate to endocrine 7, neuro 9, and Gl 8
• The remainder of the questions will relate to other modules with some crossover
• Case studies will be like the Midterm with questions related to the scenario.
• Question types include: matching, select all that apply, select "n", multiple dropdowns, multiple choice
• The time limit is 90 minutes
• Students cannot leave the room for any reason once the exam begins
• At the 60-minute mark, the exam will be paused, and students who have finished can leave
• Faster test-takers encouraged to sit at the back or ends of rows for easier exit
• Final exam grades will be released at the end of the day
• One-on-one exam reviews will be available in the summer semester if desired

About The Review

• Shock is not included in this review
• Use the shock module, class slides, and Shock Synthesis Assignment for shock content on the final exam
• Other than shock content, this review is inclusive of all concepts/conditions one will be responsible for on the final exam
• Review Synthesis Assignment 1, pre- and post-module worksheets, class slides with answers, and exam prep sections in modules.

Importance of ATP and Oxidative Phosphorylation

• Oxidative metabolism (oxphos) produces 95% of ATP
• Oxidative metabolism produces 20 times more ATP compared to anaerobic metabolism
• Zero oxygen results in less energy and more waste in the form of lactic acid

Acid/Base Balance

• Study interpretation
• Study common conditions associated with imbalances
• Study effects of imbalances on oxygen-hemoglobin dissociation curve

Metabolic Acidosis

• Occurs from excessive build-up of acid OR excessive loss of bicarb
• Use anion gap to help determine underlying cause
• pH: Low
• CO2: OK
• HCO3: Low

Anion Gap and Metabolic Acidosis

• The anion gap is the difference in cation and anion ratios in the plasma.
• It tells one if metabolic acidosis is acid build-up (H+) or loss of bicarb (HCO3).
• The normal anion gap ~ 12 mmol/L.
• Normal Anion Gap results from too little or loss of bicarb.
• Normal Anion Gap is caused by chronic diarrhea, pancreatic issues, and renal tube acidosis.
• Elevated Anion Gap is from excessive build-up of acid.
• An Elevated Anion Gap can be caused by lactic acidosis, ketoacidosis, and other renal failures.
• Medications and inherited metabolic disorders also may result in an elevated anion gap.

Metabolic Alkalosis

• Is caused by a loss of acid from blood, resulting in an excess of bicarb
• Excessive vomiting is most common cause
• Hyperaldosteronism and diuretic medications can cause Metobolic Alkalosis
• pH: High
• CO2: OK
• HCO3: High

Respiratory Acidosis

• Is caused by excessive build-up of carbon dioxide
• Hypoventilation caused by medications, drugs, and CNS depression can cause Respiratory Acidosis.
• Diffusion issues and obstructive disease can also cause it
• pH: Low
• CO2: High
• HCO3: OK

Respiratory Alkalosis

• Is caused by excessive loss of CO2
• Hyperventilation is the most common cause
• Altitude sickness and panic attacks can cause hyperventilation
• pH: High
• CO2: Low
• HCO3: OK

Understanding 02 Carrying: Vocabulary

• PaO2 = Partial pressure of oxygen
• Refers to Oxygen content dissolved in arterial blood
• Measures how well O2 moves from lungs to bloodstream for body transport
• Oxygen saturation (O2 sat, SPO2)
• Measures the % of hemoglobin (Hgb) sites in the blood that are carrying oxygen relative to all Hgb
• E.g., SPO2 of 99% = 99% of available Hgb sites are saturated with 02
• O2 Affinity
• This is how much hemoglobin wants to bind oxygen to itself
• Higher affinity = more binding of O2, less letting it go into tissues

Oxygen-Hgb Dissociation Curve – Right Shift (Decreased Affinity)

• Oxygen leaves hemoglobin and goes to the tissues in cases of acidosis
• This includes lactic acid production, other acid production (e.g. DKA) OR loss of bicarb (e.g. diarrhea), CO retention in lungs and/or being produced in excess
• Oxygen will seperate from the hemoglobin during high temperature.
• Hemoglobin has a decreased affinity for oxygen in these circumstances.
• Oxygen is more available to the tissues where it's needed.
• It makes it less likely to pick up oxygen in the lungs and take it to where it's needed, resulting in hypoxia.

Oxygen-Hgb Dissociation Curve – Left Shift (Increased Affinity)

• Oxygen will stay with or go to hemoglobin when there is alkalosis, e.g. vomiting
• Oxygen will stay with or go to hemoglobin during low temperature
• Oxygen will stay with or go to hemoglobin during low partial pressure of CO2
• Hemoglobin has an increased affinity for oxygen under these circumstances.
• It is more likely to bind to oxygen and stay with it
• It makes it difficult for oxygen to leave and go to the tissues where it's needed, resulting in hypoxia.

Fluid Filtration and Reabsorption at the Capillaries

• Filtration: movement of fluid moving OUT OF the vascular space (capillaries)
• Major force is capillary hydrostatic pressure, which pushes fluid out of the capillary
• Reabsorption: movement of fluid moving BACK INTO the vascular space (capillaries)
• Major force is capillary oncotic pressure which pulls fluid back into the capillary
• Albumin is the protein mainly responsible for this force and is made in the liver
• There is always a net filtrate (left over fluid in the interstitial space)
• The lymph system drains excess filtrate out of the interstitial space

Mechanisms of Edema Formation

• Decreased synthesis of plasma proteins (cirrhosis, malnutrition)
• Increased loss of plasma proteins (nephrotic syndrome)
• Increased plasma Na+ and H₂O retention (dilution of plasma proteins)
• Decreased capillary oncotic pressure
• Lymph obstruction
• Increased capillary hydrostatic pressure (venous obstruction, salt and water retention, heart failure)
• Increased capillary permeability (burns, inflammation)
• Loss of plasma proteins to interstitial space
• Increased tissue oncotic pressure
• Decreased transport of capillary filtered protein

The Renin-Angiotensin-Aldosterone System

• ↓BP, ↓ECF, ↓ Serum Na+, ↑ Urine Na+ cause the process to begin
• Renin is released by the kidneys, acting on angiotensinogen
• Angiotensin I turns to Angiotensin II due to the Angiotensin-converting enzyme in the lungs.
• Angiotensin II and Aldosterone causes Vasoconstriction which increases blood pressure
• This results in increased sodium and water retention
• Increasing Extracellular fluid

RAAS and Hypertension

• In healthy people, the RAAS is an important mechanism to maintain balance BP and tissue perfusion
• In hypertensive people, the RAAS can be overactive
• This can lead to salt and water retention and increased blood vessel tone.

ADH (Antidiuretic Hormone) System

• Volume receptors and brain osmoreceptors detect changes
• This influences thirst and fluid intake
• Affects Pars nervosa of posterior pituitary
• Causing increased or decreased levels of ADH
• ADH affects renal water retention and plasma osmolality

Red Blood Cells and Anemia

• Red blood cells are made in the bone marrow.
• Erythropoietin (EPO) made in the kidneys stimulates their production
• Anemia can develop from lots of reasons like iron deficiency, B-12 deficiency, hemolysis, cancers, SCD, bleeds, renal disease, and liver disease
• Signs and Symptoms can be explained when one knows what RBC's do
• Common Symptoms incude Fatigue, Tachycardia, DOE, Diaphoresis, Leg cramps, and Insomnia
• Diagnosis: CBC will determine Hemoglobin levels, Hct (Hematocrit), MCH, MCV, and RBC count
• Iron levels are important

Anemia Classification

• Microcytic hypochromic = small cell size, low color
• This is primarily caused by iron deficiencies and small, chronic bleeds
• Macrocytic normochromic = large cell size, normal color
• A lot of other nutritional deficiencies such as B12
• Normocytic normochromic = normal cell size, normal color
• This is primarily caused by blood loss

Components of Clotting

• One component of the system is the plasma
• Clotting prevents spread of infection to other tissues
• Clotting traps microorganisms and foreign bodies at inflammation sites
• Clotting forms a clot to stop bleeding
• Fibrin is the end product
• Fibrin provides the framework for future repair

Clotting Factors

• All factors are made in the liver, EXCEPT factor 8
• Factor 8 is produced by endothelium.
• Low or missing clotting factors = increased risk for bleeding
• Measure with PT/INR and PTT
• PT/INR measures extrinsic pathway
• This is helpful to determine the effectiveness of warfarin (an anticoagulant)
• PTT measures intrinsic pathway
• This is helpful to determine the effectiveness of heparin (an anticoagulant)
• Each test measures specific clotting factors to help figure out if factors are missing

Sickle Cell Disease

• Autosomal recessive disease that is inherited
• Proteins undergo polymerization, resulting in the sickling of RBCs.
• Symptoms: bilateral pain, extremity edema, acute chest syndrome, glomerular disease, and infection.
• Sickled erythrocytes regain normal shape during Reversal of hypoxemia (reoxygenation, rehydration)
• Hypoxemia, decreased pH, low temperature, and/or decreased plasma volume occurs
• Persistent hypoxemia causes further reduction in PO2 in the microcirculation; erythrocytes sickle
• Sickled cells slow blood flow, promote hypoxemia, and increase sickling
• Decreased blood pH decreases hemoglobin's affinity for O2; PO2 drops, increases sickling

Immunity Characteristics

Inflammatory Response

• A second line of defense, consisting of Neutrophils, macrophages, dendritic cells, mast cells, etc
• Histamine, Pro-inflammatory cytokines, and Other chemical messengers play vital roles
• Vascular dilation results in increased capillary permeability and pain, swelling, redness, and heat
• Also, there is a Clotting cascade, Bradykinin, and Complement

Functions of Antibodies

• Direct protection includes:
• Neutralization, which are secreted into blood and mucosa, and bind to and thus, inactivate the pathogen
• Agglutination, to cause pathogens to clump together and makes removal by phagocytosis more efficient
• Precipitation, and makes a soluble antigen into an insoluble precipitate
• Indirect protection includes:
• Complement activation → bacterial destruction by lysis
• Opsonization, which helps phagocytes recognize what needs to be eaten

Mechanisms of Immune evasion

• Protective coating to mimic "self"
• Rapid replication
• Endocytosis
• Inhibit lysosome binding
• Lyse phagocyte cellular membrane
• Inactivate digestion

Endotoxic Shock

• A specific form of Septic Shock caused by LPS endotoxins
• It is caused by a Gram-negative bacterial infection producing endotoxins from LPS on cell wall.
• This results in a Massive production of cytokines
• It is also characterized by Inflammatory tissue injuries and Multi-organ failure.
• NO, PAF: other mediators can lead to fever and other effects.

Viral Infections

• These infections need host cell DNA to replicate
• They invade the cell
• HIV infects CD4+ lymphocytes
• AIDS diagnosis at CD4+ count < 200 cells/mm3
• This can cause Anorexia, weight loss, Kaposi sarcoma, herpes lesions, cytomegalovirus retinitis, thrush (candida albicans), etc.

Hypersensitivity Reactions

• Can manifest as Auto-immune conditions
• They can be Antibody-mediated (humoral)
• Type I: allergies, anaphylactic reactions
• Type II: tissue-specific reactions of antigens binding to antibodies
• Type III: antigen-antibody complexes deposit in vessel walls or extra-vascular tissues
• Type IV: cell-mediated reactions

Type I Hypersensitivity Reaction: Anaphylaxis

• It is Mediated by IgE
• Allergy reaction Anaphylactic reaction
• Antigen from allergen causes either Mast cell or eosinophils to “de-granulate"
• The Immediate response takes about 5-30 minutes after exposure.
• This involves IgE released by B cells, release of histamine from mast cells, and Eosinophil recruitment.
• The delayed response takes about 2-8 hours after exposure and involves Leukocyte infiltration and Prostaglandin.
• Effects include Decreased blood pressure, Swelling, redness, and Bronchospasms.

Other Hypersensitivity Reactions

• Myasthenia gravis (Type II): Antibodies attack acetylcholine receptors, causing Muscle weakness
• Goodpasture's (Type II): Antibodies attack basement membrane of lungs and kidney, causing Dyspnea and renal issues including hematuria
• Reynaud's (Type III): Lack of blood flow typically to hands in response to cold, Usually resolves with warmth
• SLE (Type III): Antibody/antigen complexes in health tissue throughout body. Commonly characterized by Butterfly rash, aches, pains, and renal failure
• Type IV HSR: Delayed response that is Cell-mediated NOT antibody mediated

Cardiac Terms

• Preload: filling pressure during diastole (filling) which is affected by blood volume and pressure.
• Contractility: how well the heart can contract
• Afterload: the pressure the heart needs to push against to get blood out of the heart during systole such as SVR
• Left ventricle = highest pressure as blood is going to the whole body
• Cardiac output = Stroke volume x heart rate (CO = SV x HR) Stroke volume is impacted by preload, contractility, and afterload

Coronary Artery Disease

• Any vascular disorder that narrows or occludes the coronary arteries.
• An imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients
• Reversible myocardial ischemia or irreversible infarction may result
• The most common cause is Atherosclerosis: cholesterol engulfed by macrophages causing plaque formation in blood vessel walls
• Can form in any blood vessel in the body
• Narrows and hardens the vessel AND obstructs blood flow leading to ischemia and/or infarction

Hypertension

• Genetics, Environment, Dysfunction of the SNS, RAAS, and Inflammation are all factors in Hypertension
• Vasoconstriction and Renal salt and water retention are both primary causes
• Leading to increased peripheral resistance and an increased blood volume
• Sustained hypertension

Right Sided Heart Failure vs Left Sided Heart Failure

• Cor Pulmonale can be caused by COPD and other progressive lung diseases
• Left Sided Heart Failure presents as Paroxysmal Nocturnal Dyspnea, Elevated Pulmonary Capillary Wedge Pressure, Pulmonary Congestion, and Cyanosis.
• Right Sided Heart Failure presents as Fatigue, Enlarged Liver & Spleen, Distended Jugular Veins, Anorexia & Complaints of GI Distress, and Dependent Edema.

Atelectasis

• Collapse of alveoli caused by Reduced alveolar ventilation
• Air inside a plugged alveolus gets absorbed the alveolus collapses
• Risk factors include confinement to bed, infections, disease, foreign body
• Can lead to hypoxia, pneumonia, and respiratory failure
• Results in dyspnea, tachycardia, cough, pain, cyanosis, and wheezing
• To prevent, conduct in-hospital nursing interventions

Pulmonary Embolism Risk: Virchow's Triad

• Triad consists of (1) Venous stasis (2) Vessel injury (3) Hypercoagulability
• Leads to the formation of a Thrombus which is eventually dislodged.
• This clogs part of the pulmonary circulation
• Leading to Hypoxic vasoconstriction, Decreased surfactant, Release of neurohumoral & inflammatory substances, Pulmonary edema, and Atelectasis
• Resulting in numerous negative symptoms and potentially Shock.

Pneumonia

• Infection of the lungs
• Can be viral, bacterial, or fungal
• Causes purulent fluid in alveoli
• Can occur as Lobar (one or more whole sections of lungs) OR Bronchial (patches throughout both lungs)
• Carries Risks for those > 65 years and < 2 years of age.
• Smoking and being unvaccinated are also risks.
• Symptoms are Cyanosis, Purulent cough, Fever, Fatigue, Tachypnea, and Chest pain

ALI/ARDS

• ALI = Acute Lung Injury; ARDS = Acute Respiratory Distress
• Acute inflammation from trauma/infection
• This is characterized by a Disruption of the alveoli epithelial lining and the capillary endothelial lining.
• These factors contribute to a High mortality rate and sepsis.

Asthma In Summary

• Asthma is a Chronic inflammatory obstructive lung disease
• There are periods of no symptoms with "attacks” caused by allergen/irritant
• Asthma causes bronchospasms, airway inflammation, and mucous production = narrowed airways
• Results in wheezing, dyspnea, anxiety, coughing, chest tightness/pain, and decreased FEV1

COPD: Chronic Obstructive Pulmonary Disease

• Encompases Umbrella term for progressive obstructive lung diseases like Chronic bronchitis, Emphysema, and Refractory asthma"
• Associated with long term exposures/risks: smoking, environmental exposures, obesity, >40 years old, and a family history
• A possible cause is Rare "genetic COPD": alpha1-antitrypsin deficiency
• COPD often causes permanent functional impairment of lungs and is the 4th leading cause of death in U.S.

Emphysema Vs Blue Bloater

• Patients with "PINK PUFFER" and and high CO2 Retention
• Minimal Cyanosis; Patients often Purse Lip Breathe to compensate
• Patients with "BLUE BLOATER" have significant Airway Flow Problems
• These patients often have Color Dusky skin, lots of Recurrent Cough, can be Hypoxic.

Renal/Urinary Tract Functions

• Filter blood for waste and water
• Secrete substances from the blood and into the nephron
• Reabsorb substances from the nephron and back into the blood
• Produce hormones like Renin and EPO
• Excrete urine from the body
• Reabsorbs Water, Glucose, Amino acids, and Electrolytes
• Secretes Urea and H+

Acute Kidney Injuries

• A marked Decrease in GFR causes low urine output and accumulation of nitrogenous wastes in the blood
• Tests include kidney function measurement through BUN and creatinine.
• A common cause is Pre-renal: inadequate perfusion due to low cardiac output and low blood pressure
• Intra-renal/Intrinsic causes occur the kidney/nephrons themselves are injured/not working properly
• Post-renal: obstructions and stenosis

Chronic Kidney Disease

• Causes a Progressive loss of renal function associated with systemic diseases.
• Diabetes mellitus is a signifcant risk factor, including hypertension, systemic lupus, or intrinsic kidney disease
• Kidney patients exhibit Symptoms of increased levels of creatinine, urea, and potassium
• Alterations in salt and water balance usually do not become apparent until remaining renal function declines to less than 25%

Clinical Manifestations of CKD

• Azotemia: increased levels of serum urea, serum creatinine, and other nitrogenous compounds related to decreasing kidney function.
• Uremia: pro-inflammatory state with many systemic effects.
• Common Symptoms affect many functions.

Thyroid and Parathyroid Conditions

• Study Hypothyroidism (Primary vs. secondary)
• Study cause and S/S of Hashimoto's
• Study cause and S/S of endemic goiter
• Study Hyperthyroidism (Primary vs. secondary)
• Study cause and S/S of Grave's with thyroid crisis storm
• What does parathyroid hormone do?
• What will you monitor?
• When does hypoparathyroidism most likely occur?

Adrenal Crisis

• Adrenal Crisis is a Life-threatening condition
• It is Severe acute adrenal insufficiency of cortisol/aldosterone
• It can be caused by Trauma, Addison's disease, or Pituitary injury
• It can be caused by dehydration or physiological stress, AND Sudden discontinuation from glucocorticoids

Adrenal Crisis: Signs and Symptoms

• It manifests as Acute Shock that doesn't respond to fluids or medications
• With common symptoms such as low blood pressure, tachycardia, weakness, and fatigue
• Patients may exhibit a Decreased appetite, Orthostatic hypotension, or Electrolyte imbalances

Diabetes Mellitus

• Type I: autoimmune destruction of beta cells in pancreas due to some trigger
• Patients cannot make insulin and Need Insulin for body to get glucose into cellls
• DKA is always a danger with type I
• Type II: insulin resistance where the PANCREAS IS FINE yet patients are resistant to insulin
• High insulin wears out beta cells and DKA can occur

Complications from Diabetes: DKA (Diabetic Ketoacidosis)

• Lack of insulin glucose can't get into the cell starving cells + high BG
• Fat is broken down for fuel → ketone production → ketones in urine Symptoms: Fruity-scented breath, N/V, polyuria/polydipsia, fatigue, confusion coma/death
• At risk:
• Type 1 or insulin-dependent diabetes patients
• Ptients with high blood glucose

From Where is the Bleed?

• Upper GI Tract is Proximal to the Ligament of Trietz
• Hematemesis (Upper Gl) from Frank blood or Coffee grounds
• Melena (Upper and Lower) presenst as Black or maroon stools
• Hematochezia (is Low or Massive Gl) and creates blood streaking
• Occult (can be anywhere) is Asymptomatic with Normal Stools
• If found often in older adults, they are anemic

GI Disorders

• Mallory-Weiss tears: vertical, shallow tears in esophagus causing bleeding; typically from vomiting
• GERD and Barrett's esophagus manifest with cellular adaptions
• Mechanical obstructions Intussusception: telescoping bowel obstruction
• Volvulus: twisted intestine
• Herniation: piece of bowel slips in between a tear in a muscle
• Adhesions: scar tissue formation

Crohn's vs UC

• Crohn's: Skip lesions with Small/large intestine affectation
• Transmural inflammation can lead to fissures
• Ulcerative colitis is Large intestine continuously affected Pseudopolyps and Mucosal/submucosal ulcerations

Portal Hypertension and Ascites

• Cirrhosis is a leading cause leading to high resistance to flow
• This results in portal hypertension
• Decreases Albumin leveles
• Which lowers oncotic presssure
• Causes more congestion and pooling
• The use of diuretis is sometimes effective

Portal Hypertension and Varices

• Dilated submucosal veins in lower 1/3 esophagus are secondary to portal HTN
• It is primarily caused by cirrhosis
• Asymptomatic unless a vessel ruptures
• This rupture causes Hematemesis, melena, and shock, ultimately leading to death

Types of Jaundice

• Three types of jaundice
• Hepatobiliary mechanisms
• Intrahepatic obstructive jaundice
• Extrahepatic obstructive jaundice
• Hematologic mechanisms
• Hemolytic jaundice

Cerebral Vascular Disease

• It is the Most frequently occurring neurologic disorder caused by pathology is the blood vessels
• It is Caused by Vessel wall damage, occlusion and rupture, AS WELL AS abnormalities is the blood

TIA's vs. Strokes

• Transient Ischemic Attack (TIA. TIA) episodes of dysfunction lasting for no more than 1 hour.
• Results from focal ischemia.
• 17% of patients with TIA will exhibit a stroke within 90 days
• Stroke, CVA (Cerebral vascular accident):
• A potential sign is that Neurons undergo changes that disrupt plasma membranes
• Patients may experience motor, speech, or swallowing problems

Other Neuro Conditions

• Be aware of symptoms of Seizures (Generalized vs. focal)
• Be aware of symptoms of Triggers
• Recognize the significance of intracranial pressures in Hematomas
• Study Whats a brain herniation?
• Understand diagnosis and trearment of Parkinson's: dopamine deficiency, tremor, bradykinesia, and cogwheel rigidity
• Know the signs and symptoms of mild, moderate, and severe TBIs

Comparison of Delirium and Dementia

Other Concepts/Topics

• Study SNS activation and Compensatory mechanisms for hypoxemia/hypoxia
• Be aware of which products are made where (such as albumin, clotting factors, EPO, ADH, etc.)
• link with Signs/Symptoms of acute and chronic conditions