Exam 1 Patho

Pathophysiology

Study of disease, causes, changes in body, signs/symptoms

Etiology

The cause/origin of a disease (genetic/environmental), why a disease develops

Pathogenesis

Steps in the development of disease, how a disease develops

Acute

Disease that is short term, arises and quickly resolves (6 months)

Chronic

disease that often has less notable signs/symptoms that occur over a long period of time. 

Homeostasis

refers to equilibrium, balance, stability in the body. CELLS, TISSUES, ORGANS NEED STABILITY to FUNCTION NORMALLY

Manifestation:

clinical effects or evidence of disease; signs (what is seen or measured) and symptoms (what patient describes but is not visible)

Idiopathic

no known single cause 

ex. Hypertension, could be alcohol or stress

Iatrogenic

disease/condition we cause patients because of our care/interventions

Cytoplasm

Liquid with water, nutrients, ions, dissolved gasses, and wast product; where cellular work occurs

Organelles

Perform the work that maintain a cell life

Nucleus

Control center of the cell; regulates cell growth, metabolism, and reproduction; some drugs work by entering nucleus, attaching to DNA, and disrupting cell growth

Cell Membrane

Phosopholipid bilayer, permeable to some molecules but not to others. studded with many different protein channels and receptors; drugs bind to these receptors

Diffusion

Movement of solute from high to low concentration; no need for energy

Ex. exchange of gasses in the lungs

Osmosis

Movement of water/solvent from a low solute concentration to a high solute concentration; no need for energy

ex. in kidneys

Facilitated Diffusion

Movement of solute from higher to lower concentration with assistance of a carrier molecule; no need for energy

ex. insulin transporting glucose inside of cells

Active Transport

Movement of a solute from an area of lower concentration to higher concentration; need energy

ex. sodium potassium pump

Where are Potassium and sodium moving with Na/K pump? Why is energy required? and what form of transport it is

Sodium is moved out of cell, Potassium is moved into cell; needs ATP to maintain right concentration of ions and molecules; its Active Transport

Energy Source to make ATP

Glucose and Triglycerides; larger molecules are stored until needed or metabolized

What happens to Triglycerides during starvation state?

glycerol used to create glucose for brain/blood cells; Fatty Acids used to create Ketone bodies for fuel 

If no oxygen after glycolysis, pyruvate becomes?

lactic acid, only ATP generated

If oxygen is present after glycolysis, pyruvate becomes?

Acetyl CoA, enters Kreb’s Cycle → ETC for lots of ATP

How much ATP is produced from ETC?

net 34 ATP

What does Hypoxia cause?

Low oxygen in blood → low oxygen in tissue → body more acidic

What are some reasons for low oxygen levels?

Asthma Attack: inflamed small airways, cant get oxygen into bloodstream

Hemorrhage: Losing RBCs from body & RBCs carry hemoglobin, the protein responsible fro oxygen transport = diminished oxygen-carrying capacity

Anemia: Lack of blood; low iron; low hemoglobin; diminished capacity to carry oxygen

What does a patient get stuck in when they have diminished oxygen levels in the blood? what does this generate?

They get stuck in glycolysis, generating a limited number of ATP and excessive amounts of lactic acid

What is lactic acid buildup a result of? what is a waste product of ATP production? What lab results will see from a recently resuscitated individual?

Lactic acid buildup is a result of hypoxemia;

Carbon Dioxide is a waste product of ATP production;

High lactic acid, low pH, High Carbon dioxide, High Potassium

Type 1 DM

Usually acute onset before the age 30, Lack of Insulin, needs insulin injections

Type 2 DM

After age 30 gradual progression, insulin resistance + inadequate production, needs PO meds and lifestyle

Normal blood glucose range

77-99 mg/dL

What does the Insulin hormone do?

Lowers blood glucose by facilitating glucose entry into cells

What does the Glucagon hormone do?

Raise blood glucose levels by converting glycogen into glucose in the liver

What does the Pancreas do as an exocrine/endocrine gland

Exo: Secretes pancreatic enzymes

Endo: Secreted hormones into the bloodstream

What are GLUT receptors?

Proteins that transport glucose into cells (Facilitated Diffusion)

where are GLUT4 receptors found?

Insulin-dependent, muscle, liver, fat cells

How does T1DM insulin shots work?

Give more insulin

How does T2DM PO meds work?

Makes tissues more responsive to insulin

How do we diagnose a Fasting blood glucose diabetic?

126 mg/dl or greater

How do we diagnose a Glycated or Glycosylated hemoglobin (A1C or HbA1C) test diabetic?

indicates average blood sugar level for the past three moths, an A1C of 7% or above = poorly controlled blood sugar 

S/S of hyperglycemia

Polyuria (large urine product), Polydipsia (more fluid intake), Polyphagia (increased appetite)

S/S of hypoglycermia

<60mg/dl, tachycardia (fast heartbeat), Diaphoresis (excessive sweating)

15/15/15 Rule

15 grams of fast-acting carbs

wait 15 minutes and check blood sugar

more 15 grams if blood sugar less than 70

Benign Growth

Mirrors original cell, but cant spread to other organs

Malignant Growth

abnormal cells, invade tissues/organs, spreads

How genetics connect to healthcare

Health problems are due to genetic mutations.

Dominant allele

a gene that expresses its trait, or phenotype, even when only one copy is present

Recessive allele

a gene that only expresses its trait, or phenotype, when two copies are present.

Phenotype

Observable traits

Genotype

Actual allele combination

Autosomal dominant

trait appears every generation; dominant allele paired with recessive

Autosomal recessive

trait may not appear every generation; only when both alleles present

Sex-linked recessive

the gene allele present on both x chromosomes (2 females, 1 male)

Complex/multifactorial inheritance

health problems appearing within family but no pattern 

Variation

when people have different sequences compared to wild-type (normal). This could affect risks or resistance to drugs or diseases.

Mutation

base differences results in loss of protein functioning leading to impaired cell

What is CYP450, and why is it important?

An enzyme in the liver used in toxin and drug motablism; it affects drug metabolism speed and response. 

What causes cystic fibrosis?

Mutation in CFTR gene → defective chloride channel → thick mucus in lungs/pancrea

What is Adaption?

cells trying to change their own death/adapt from environmental changes

Atrophy

Decreased work demands on the cell. Decreases in size (organelles too) and numbers, uses less oxygen,

Causes: denervation, inadequate nutrition, ischemia, etc.

Hyperplasia

the increase in number of cells in an organ/tissue

Hypertrophy

Increased in cell size in an attempt to meet increased work demands

Metaplasia

when one adult cell is replaced by another

Dysplasia

abnormal and rapid changes in cells size, shape, and loss of cellular organization

What is Necrosis?

Premature death of cells in living organism by autolysis; triggered by poison, lack of blood flow, infection, tissue hypoxia

Cell doesn’t respond to it normally as it doesn’t clean it up, but lets it decompose

Coagulative Necrosis

interruption in blood flow - when this happens pH drops (Heart, Liver, Kidneys)

Gangrene

Impaired blood flow and bacterial invasion

Dry Gangrene

Bacterial load is low, skin is dry/dark brown/black

Gas Gangrene

Clostridium bacteria, releases gases

Wet Gangrene

damage from bacteria, WBC produce a liquid wound

Apoptosis

Programmed cell death, gene activation, DNA damage, lack of hormone stimulation, affects single or small group

Compartment syndrome

Increased pressure in a muscle compartment

Caused by trauma, crush injury, burns, etc.

Smooth Muscle 

Involuntary, GI tract, vessels

Cardiac Muscle

Involuntary, striated, heart

Skeletal Muscle

Voluntary, striated

What is pharmacology?

The study of how drugs are administered, where they travel in the body, and the responses they produce (intended and unintended).

What is a drug?

A chemical agent that produces biological responses in the body (intended or unintended).

What is mechanism of action (MOA)?

How a drug produces its physiological effect (e.g., opioids bind to mu receptors to decrease pain).

What is a drug category?

Larger grouping of drugs with the same therapeutic effect (e.g., analgesics, anticoagulants).

What is a drug class?

Smaller group within a category; drugs share chemical structure or MOA (e.g., opioids vs NSAIDs within analgesics).

What is a prototype drug?

Well-understood, representative drug in a class (e.g., Morphine for opioids).

What is bioavailability?

Extent/rate a drug reaches systemic circulation and acts on target tissues.

What is drug specificity?

Ability of drug to bind to specific receptors; opioids bind mu receptors → pain relief, but also constipation (universal).

What are the common side/adverse effects of opioids?

Constipation (universal), sedation, confusion, respiratory depression, urinary retention.

How to identify opioids?

Names often include “morph,” “cod,” or “oxy” (e.g., codeine, oxycodone, hydrocodone, hydromorphone).

Difference between chemical, generic, and trade names?

Chemical = scientific name (NaCl, KCl). Generic = official name (acetaminophen). Trade = brand name (Tylenol).

Prescription vs OTC drugs?

Prescription requires order from provider; OTC considered safe without supervision.

What is teratogenicity?

Ability of drug to cause fetal harm. Categories: A = safe, B–D = increasing risk, X = contraindicated.

Which DEA schedule has highest abuse potential?

Schedule I (heroin, LSD, ecstasy, peyote); no accepted medical use.

Which DEA schedule has lowest abuse potential?

Schedule V (some cough medicines, anti-diarrheals).

What is tolerance?

Decreased response to drug over time → requires higher dose.

What is drug sensitivity (cumulative effect)?

Body cannot metabolize/excrete a dose before next one; effects accumulate (common in liver/kidney impairment).

What is drug toxicity?

Excessive dose or impaired clearance → drug buildup, toxic effects (e.g., acetaminophen → liver damage).

What do nurses need to know before giving a drug?

Drug name (generic/trade), intended use, MOA, therapeutic effect, contraindications, side/adverse effects, how to administer, nursing implications.

What’s the difference between side effect and adverse effect?

Side effect: anticipated, usually mild (e.g., ondansetron → sedation). Adverse effect: harmful, serious, often unexpected (e.g., alteplase → hemorrhage).

What is an allergic reaction?

Immune hyperresponse to foreign substance; histamine release causes hives, itching, tearing, localized edema.

What is anaphylaxis?

Severe allergic reaction → systemic histamine release → hypotension, airway compromise, hypoperfusion, multi-organ shock.

What are key anaphylaxis symptoms?

Hypotension, wheezing/dyspnea, angioedema, confusion, loss of consciousness, cardiac arrest.

What are the 6 rights of medication administration?

Right dose, right route, right time, right patient, right medication, right documentation.

What are the 3 checks of drug administration?

Check MAR when removing drug, check drug when preparing, check before administering to patient.

Examples of high-alert medications?

Epinephrine, Warfarin, Heparin, Insulin, Magnesium sulfate, Potassium chloride, Oxytocin.