NUR 2108 Human Pathophysiology Final Exam

Explain the pathophysiology of Chronic Bronchitis (COPD)

1. Smoke and irritant exposure cause airway mucosal inflammation

2. Globulet cell hyperplasia (increase) and mucous gland hypertrophy (grows larger)

3. Mucociliary clearance impairment leads to mucus plugging

4. Airway wall edema and smooth muscle hypertrophy lead to an increase in resistance

5. Chronic hypoxemia causes hypoxic pulmonary vasoconstriction, leading to Pulmonary Hypertension

6. Increased Erythropoietin causes polycythemia (increased RBC), which ultimately causes cyanosis, RV hypertrophy, and all cause cor pulmonale

Hallmark Symptoms

Chronic bronchitis is a productive cough lasting for longer than 3 months in a year, for two consecutive years.

Primary defect is airway inflammation and mucus, NOT alveolar destruction like emphysema

Hypoxemia is severe and early; look for hyperventilation and CO2 retention

Blue Bloater: Decreased PaO2, increased PaCO2 , polycythemia, peripheral edema

Most COPD patients will have BOTH components

Pathophysiology of COPD Emphysema?

Alveoli walls break down—surface area for respiratory exchange is greatly reduced
• Lungs lose elasticity
• Results in air being trapped in lungs, reducing effectiveness of normal breathing

Hallmark Symptoms of Emphysema

Alveolar Destruction: decreased surface area causes decreased DLCO

Loss of elastic recoil: dynamic collapse on expiration

Hyperinflation: Increased functional residual capacity (FRC), which means air trapping, causing barrel chest

Pursed-lip breathing: helps maintain airway pressure, slows collapse

Pink Puffer: hyperventilation of the lungs to maintain PaO2 — not hypoxic until late in the disease

Cor pulmonale (late): hypoxic vasoconstriction leads to pulmonary hypertension, leading to RV failure

Explain the pathophysiology of Pnemonia

Pneumonia is consodilation, impaired gas exchange

Pathogen reaches alveoli (aspiration, inhalation, hematogenous) causes bacterial Pneumonia, which causes systemic fever, increased WBC, and cytokine release, all of which increase the risk of sepsis if bactremia

Ventilation and Perfusion in Pneumonia

Ventilation-perfusion mismatch that often progresses to a true intrapulmonary shunt, deoxygenated blood enters the blood stream —> Hypoxemia

Basic Principles around the spread of Tuberculosis (TB)

TB is spread by Airborne droplet nuclei (not droplets)

In Latent TB: not infectious, Positive TST/GRA, normal CXR

Active TB: Symptomatic and CXR Cavitation, needs mandatory reporting

Underlying Pathophysiology of Pulmoary Fibrosis:

Restrictive Lung Disease, triggered by repetitive epithelial injury like toxins, dust, autoimmune, or idiopathic

Abnormal wound healing leads to fibroblast proliferation and an excess of collagen deposition

The alveolar wall thickens, decreasing compliance, making breathing more difficult

Decreases diffusion capacity, causes hypoxemia with exertion, and then eventually at rest.

S/S honeycombing, pulmonary HTN, cor pulmonale

What are the expected laboratory abnormalities in a patient with chronic renal failure?

High phosphorus and potassium, low calcium, anemia, metabolic acidosis

What is a UTI?

Cystitis: the infection stays within the bladder

S/S Dysuria, urgency, frequency, suprapubic pain

No Fever

E. Coli

Short female urethra = increased risk; caused by sexual activity or catheters

What is Pyelonephritis?

Technically an “Upper UTI”

Infection reaches the kidney, causing systemic response

Fever present

Urosepsis if untreated

Recurrent, cortical scarring, decreased GFR over time

How do different types of AKi Occur: Prerenal

In Prerenal AKI: not enough blood is getting TO the kidney

How do different types of AKi Occur: Intrinsic AKI

In Instrinsic AKI, there is damage to the kidney tissue itself

How do different types of AKi Occur: Postrenal AKI

In Postrenal AKI: Urine can’t get OUT of the kidney

Nephrotic Syndrome:

Filter is LEAKY, protein is pouring out

Key finding is massive proteinuria (>3.5g/day)

Edema caused by decreased albumin causing decreased oncotic pressure which leads to fluid leaking into tissue

High cholesterol due to liver making lipoproteins compensate for lost protein

Little to no Hematuria

Minimal Change Disease in kids, FSGS Membranous in adults

Oval fat bodies

Nephritic Syndrome

Filter is INFLAMED, blood leaks out

Key finding is hematuria and RBC casts in urine

HTN is present due to decreased GFR causing sodium and water retention, increasing BP

Some proteinuria (<3.5g/day)

Post-Strep GN (children), igA Nephropathy 9young adults)

RNC casts = pathognomonic for glomerular bleeding

Proteinuria

Large amounts of excess protein being excreted in urine

S/S Edema, decreased albumin leads to a decrease of oncotic pressure, which causes fluid to leak out.

What type of WBC are elevated in Bacterial infections?

Neutrophils are elevated in bacterial infections

What type of WBC are elevared in Viral Infections?

Lymphocyetes: NK cells, T cells (CD4 and 8), and B cells.

What type of WBC are elevated in Allergic Reactions?

Basophils/ Eosinophils

Release histamine and herparin. Central to allergic reactions

What non-specific labs determine whether inflammatory or autoimmune responde is occuring?

Inflammatory: High WBC, neutrophilia reflects acute inflammatory response.

CRP rises quickly after tissue injury

ESR lags behind, reflecing susttained inflammation

Normal or low procalcitonin would argue against infection

Autoimmune: increased neutrophils, lymphocytes, eosinophils, basophils

What should granulation tissue look like?

beefy red, moist, bumpy

Why does granulation tissue look like this?

Angiogenesis forms new capillariies

Epithelial cells migrate to close the wound surface

Fibroblast produce collagen and extracellular matrix

Type 1 Hypersensitivity Reactions

IgE-Mediated (Immediate)

Occurs in minutes

IgE on mast cells causes histamine release

Eg: Anaphylaxis, Asthma, Hay Fever, Bee sting

Type 2 Hypersensitivity Reactions

Cytotoxic (Antibody Mediated)

IgG/IgM bind to cell surface antigens, causing cell destruction

Eg: Hemolytic Transfusion rxn, Good Pasture’s, myasthenia gravis

Hyperacute Transplant Rejection

Rejection within minutes to hours

Humoral (antibody mediated) — Type 2 hypersensitivity

Pre-formed recipient antibodies attack donor endothelium immediately, causing thrombosis and then ultimately organ necrosis

Chronic Transplant Rejection

Rejection in months to years

Both humoral and cell-mediated, chronic low-grade inflammation

Slow progressive fibrosis and vasculopathy from repeated subclinical immune attacks

— T cells and antibodies cause gradual scarring — chronic allograft neropathy, bronchiolitis obliterans (lung)

Which immunoglobulin is passed in Breast Milk?

immunoglobulin A (IgA) which is 10-15% of Ig, is passed in breast milk

Which immunoglobulin is passed via Placenta?

Immunoglobulin G (IgG) which is 75-80% of Ig, is passed via the placenta

Which Immunoglobulin is responsible for hypersensitivity reactions?

Immunoglobulin E (IgE) which is <0.001% of Ig, is responsible for hypersensitivity reactions. Like allergic reactions, triggering anaphylaxis

What causes autoimmune disorders?

Loss of self-tolerance causes autoantibodies and autoreactive T cells to destroy normal tissue

What serum markers are specififc for autoimmune disorders?

ESR and CRP: are nonspecific markers of inflammation, not specific autoimmune disorders

What serum is a marker for Systemic Lupus (SLE)?

Anti-dsDNA, ANA

What serum is a marker for Rheumatoid Arthritis (RA)?

Rheumatoid Factor (RF)

What serum is a marker for Chrohn’s Disease?

ASCA, elevated CRP/ESR

What type of virus is HIV?

HIV is a immunodeficiency virus

What cells does HIV Infect?

HIV destroys helper T cells over time, over time. Without CD4+, B cells can’t be activated properly.

How is the progression of HIV monitored?

1. high-risk patients screened, HIV RNA willdetect acute infection before antibodies appear

2. Then, CD4 count and viral load are monitored every 3-6 months. ART adherence is stressed, annual TB testing, routine vaccinations (no live)

3. Prophylaxis: TMP-SMX for PCP; fluconazole for fungal; ART restart after acute stabilization

Stage 1: Acute HIV Infection

2-4 weeks post-exposure

CD4: Normal >500, Viral Load: VERY High

Flu-like illness: fever, lymphadenopathy, rash, sore throat, myalgia

Mistaken for influenza or mono

HIGHLY infectious, peak transmission window

Many are unaware they are infected with HIV

Stage 2: Chronic HIV (Clinical Latency)

Months to 10+ Years

CD4 200-500 (declining) Viral Load: Low-Moderate

May be asymptomatic for years

Minor infections: oral candida, herpes zoster, recurrent UTIs

Slow decline of CD4+ cells (lose 50-100/year without ART)

On ART: viral load undetectable; near-normal life expectancy

U = U, undetectable = untransmittable

Stage 3: AIDS

CD4 <200 cells/mm3, Viral Load: HIGH

When CD4 <200 or AIDs-defining Illness

Pneumocystis jirovecii pneumonia (PCP) — most common OI

Toxoplasma encephalitis

CMV retinitis → blindness

Cryptococcal meningitis

Mycobacterium avium complex (MAC)

Kaposi sarcoma, CNS lymphoma

Who can/cannot transmit HIV?

Stages 1 and 3: HIGHLY transmissible

Stage 2 (Latency): if on ART ro make viral load undetecable, can’t transmit

Ischemic Stroke

Characterized by a blockage of blood flow to the brain from a blockage in ond of the main cerebral arteries

Account for 87% of ALL strokes

Time sensitive = Time is BRAIN

Risk Factors that contribute to Ischemic Stroke

Embolic: atrial fibrillation, clotting disorders, cancer, use of birth control, illicit drug use

Atherosclerotic/Stenosis: atherosclerosis, CAD, Hyperlipidemia, Obesity

Hemorrhagic Stroke

Characterized by a rupture of a blood vessel in the brain causing bleeding

Accounts for 13% of all strokes

Overall poor outcomes

Risk Factos that contribite to Hemorrhagic Stroke:

Hypertension: #1 cause, long-term HTN

Cerebral Aneursym: weakenng of vessel walls where aneurysm forms increasing bleeding risk

Arteriovenous Malformation (AVM): risk of rupture is high

Substance use: especially cocaine and alcohol

Recognize Stroke:

F: Facial Droop
A: Arm weakness (one sided)
S: Speech Problem
T: Time to call 911

How to recognie R versus L sided Stoke: Left

Right sided motor and sensory symptoms

Right visual cut or eye movement loss

Aphasia: speech impairment

Issues with reading or writing

How to recognie R versus L sided Stoke: Right

Left sided motor and sensory symptoms

Left visual cut or eye movement loss

NORMAL speech patterns

May be impulsive

May have more neglect

S/S Basilar/Veterbal Artery Stoke

Severe dysfunction, often complete quadriplegia, altered level of consciousness, breathing issues

What symptoms do patients present with in Transient Ischemic Attacks (TIAs)?

TIA patients can present with symptoms just like a stroke. However, they are short term and resolve without treatment. TIAs are caused by a temporary blockage of blood flow in the brain, lasting a matter of minutes to 24 hours. Puts patients at a HIGH risk for future stroke.

How is a TIA different than an Ischemic stroke?

TIAs = temporary blockage of blood flow in the brain

Ischemic Stroke = blockage of blood flow to cerebral arteries

What are seizures?

Seizures are an abnormal electrical activity in the brain that may or may not present physical symptoms

Generalized seizures vs Focal seizures?

Generalized seizures occur on both hemispheres of the brain. Ex: Tonic-clonic, myoclonic, absence

Focal seizures occur on only one side of the brain. Ex: complex partial and simple partial

Monroe Kelli Doctrine- What three componenet s make up ICP?

Brain tissue

Cerebrospinal fluid (CSF)

Blood volume

What condiitions can cause increased ICP?

Brain swelling post-injury increases pressure

Increased cerebrospinal fluid can increase pressure

Autoregulation of pressure and hemodynamics can alter ICP

(blood/masses also impact pressure)

What is Parkinson’s disease?

Disease of the central nervous system

What neurotransmitter is involved in Parkinson’s?

Severe degeneration in the substantia nigra of the basal ganglia, with loss of dopamine-producing neurons

Imbalance of Dopamine and Acetylcholine: LOW dopamine

Hallmark Symptoms of Parkinson’s Disease

Staring appearance; lack of facial expression

Specific •tremor of “pill-rolling” action of one hand common

•slowed up movements and freezing episodes: bradykinesia

•cannot initiate movements at times; vs. cannot be still

•postural imbalance

Stiffness & muscular rigidity

Dementia late in the disease

What is ALS: Amyotrophic Lateral Sclerosis

Neurodegenerative disorder involving upper and lower motor neuron structures

Causes progressive muscle weakness (motor decline)

Unknown etiology

Usually fatal from respiratory failure within 3 years of diagnosis

Cognition remains intact (no cognitive decline)

What are early signs of ALS disease?

Starts with muscle weakness, which then progresses to muscle atrophy and loss of manual dexterity

What are late symptoms of ALS Disease?

Late stages include respiratory compromise and inability to speak

What are examples of Progressive Neurodegenerative Disorders?

1. Parkinson’s Disease

2. Huntington’s Disease

3. Amyotrophic Lateral Sclerosis

What are examples of autoimmune related neurological conditions?

Multiple Sclerosis

Guilllain-Barre

Myasthenia Gravis

Myasthenia Gravis

Acquired chronic autoimmune disease

Defect in nerve impulse transmission at the neuromuscular junction

Reduces receptor availability for acetylcholine

An IgG antibody is produced against receptors

Can exacerbate in response to stressors (myasthenic crisis)

S/S of Myasthenia Graves

Bulbar weakness: issues swallowing, breathing, eye weakness. Proximal weakness is common and all symptoms can progress to acute respiratory failure

Multiple sclerosis

Chronic autoimmune inflammatory disease, causing demyelination of nerves in the CNS. Chraracteristic “plaques” or areas of demyelination occur on MRI

Disrupts nerve condcution with subsequent death of neurons and brain atrophy

Can affect sensory and motor functions

S/S of Multiple Sclerosis

First symptoms often visual or balance (cerebellar)

Paresthesia, weakness, impaired gait

Urinariy incontinence

Spastic Paralysis

Guillain-Barre Pathophysiology

Acquired inflammatory autoimmune disease that causes demyelination of the peripheral nerves.

Usually occurs following respiratory or GI virus, sometimes after vaccination

Some make a FULL recovery, recovery over weeks to months

Often characterized by ascending motor weakness

Guillian Barre Symptoms

Numbness/Tingling

Weakness starting in lower extremeties

Can progress to quadriplegia and acute respiratory failure

Autonomic nervous instability

What are three classic, non-specific signs of anemia?

Note: anemia is a sign, not a diagnosis.

1. Decreased production: bone marrow failure, iron/B12/Folate deficiency, chronic disease (decreased EPO), and aplastic anemia

2. Increased Destruction: hemolytic: intrinsic (G6PD, sickle cell), Extrinsic (autoimmune, mechanical), shortened RBC lifespan (<120 days), and increased bilirubin which causes jaundice

3. Blood loss: acute (trauma, hemorrhage), chronic: (GI Bleed, menorrhagia), depletes iron stores over time, compensatory reticulocytosis

S/S of Iron Deficiency

(Microcytic) MCV <80

PICA: abnormal cravings for non-food items with no nutritional value (clay, dirt)

Smooth and Glossy Tongue

S/S of Sickle Cell Anemia (Hemolytic Anemia)

Normocytic (MCV 80-100)

Enlarged spleen or liver

Dark, blood tinged urine (from hemolysis)

Jaundice and Fever

S/S of B12- Pernicious Anemia

Macrocytic (MCV >100)

GI Upset

Weight loss

Taste and smell changes

Beefy red tongue

Confusion

What triggers EPO release?

Hypoxia (low tissue oxygen levels) triggers the kidneys to release EPO, which stimulates RBC production in the bone marrow.

What is erythropoiesis? What crucial ingredients are necessary for erythropoiesis to occur?

Erythropoiesis is the formation of RBCs in the bone marrow and requires EPO, iron, vitamin B12, folate, and adequate protein.

Red Blood Cells (RBCs)

Carry oxygen via hemoglobin

Low levels cause Anemia

Clinical Signs: Fatigue, pallor, weakness, shortness of breath, dizziness, tachycardia

White Blood Cells (WBCs)

Fight infection and provide immunity

Low levels cause Leukopenia/neutropenia

Clinical Signs: Frequent infections, fever, poor wound healing

Platelets (Thrombocytes)

Blood clotting/hemostasis

Low levels cause Thrombocytopenia

Clinical Signs: Easy bruising, petechiae, bleeding gums, prolonged bleeding

What Lab monitors the effects of Warfarin?

PT/INR

What lab monitors the effects of Heparin/Coumadin Therapy

aPPT

If the aPPT and PT/INR are above the normal range, what does that mean?

aPPT and PT/INR too high, which means the blood is too thin and depicts a bleeding risk due to too much anticoagulation

IF a patient is sufficiently anticoagulated, we expect the PTT or PT/INR to be higher than the normal range (but not too high! ---this would increase risk for bleeding).

If the aPPT and PT/INR are below the normal range, what does that mean?

If aPPT and PT/INR are below the normal range, blood is too thick, and depicts a clotting risk

Which abnormal cell types are associated with Acute Lymphoblastic Leukemia

• Acute Lymphoblastic → lymphoblasts (B or T malignancy)

Which abnormal cell types are associated with Chromic Lymphocytic Leukemia

• Chronic Lymphocitic → abnormal B mature lymphocytes

Which abnormal cell types are associated with Acute Myelogenous Leukemia

• Acute Myelogenous → myeloblasts (auer rods on smear)

Which abnormal cell types are associated with Chromic Myelogenous Leukemia

• Chronic Myelogenous → abnormal myeloid cells/granulocytes

What abnormal cell types are associated with Lymphoma

malignant lymphocyte proliferation within lymphoid tissue

Abormal cell difference Hodgkin Lymphoma and Non-Hodgkin Lymphoma?

Hodgkin Lymphoma contains Reed-Sternberg Cells (bi-nucleiated giant B cells)

How are cancer cells different from healthy cells?

Cancer cells evade apoptosises (they refuse to die)

Angiogenesisis (new blood vessel growth feeds the tumor

Cells detatch and spread

T-cell supression allows cancerous cells to evade destruction by the immune system

What is disseminated intravascular coagulation (DIC)

DIC is a clinical emergency with 2 phases. Phase 1 massive clotting and phase 2 bleeding.

Key concept of disseminated intravascular coagulation?

Systemic trigger → widespread thrombin activation → simultaneous microvascular clotting AND factor/platelet consumption → paradoxical hemorrhage (patient bleeds BECAUSE they clotted too much)

What are the side effects of corticosteroid therapy?

Peptic Ulcer Disease, hyperglycemia, Weight gain, HTN, thrombophlebitis, thromboembolism, accelerated atherslerosis

What endocrine disorder results from chronic corticosteroid use?

Cushing’s Syndrome is caused by chronic exposure to excess corticosteroids.

What are the S/S of Hyperthyroidism?

Buldging eyes, intolerance to heat, finger clubbing, enlarged thyroid, amenorrhea, weight loss, tachycardia

Note: Thyrotoxicosis (thyroid storm)

S/S of Hypothyroidism

Intolerance to cold, receeding hairline (hair loss), facial and eyelid edema, extreme fatigue, thick tongue, muscle aches, brittle nails, anorexia,

Note complication: Myxedema Coma (hypo- progresses to mental impairment or coma)

Pathophysiology of Grave’s Disease

An autoimmune disorder characterized by enlargement of the thyroid and excess secretion of thyroid hormone

May be precipitated by

  stress 

  iodine deficiency

  infection

  smoking

  genetic factors

Alternates between remissions/exacerbations

May progress to thyroid destruction resulting in hypothyroid

What findings does the nurse expect to see in a patient with Diabetes Insipidus

Excessive fluid loss (2-10L/day)

Diluted Urine (<1.005)

Hyperosmolality (>295mOsm) lots of THIRST

Hypernatremia (> 145)

What hormone is involved in Diabetes Insipidus and what happens to it?

ADH is involved in DI. In DI, ADH is decreased, which descreased H20 absorption.

What hormones are secreted from the hypothalamus?

Releasing Hormones: CRH, TRH, GHRH, GnRH, PRF

Inhibiting Hormones: Somatostatin, PIF