Exam 2 Patho

Primary Hemostasis

first response - Primary Hemostasis: Platelet plug
(platelets stick to damaged tissue)
and vasoconstriction

Secondary Hemostasis

after primary hemostasis - Fibrin clot
(stabilizes platelet plug)

Fibrinolysis

(after secondary hemostasis) - Plasmin breaks down
fibrin, preventing the clot from
growing and becoming problematic
(preventing uncontrolled thrombosis
and embolism)

Hematochezia

Fresh (bright) red blood in the stool,
originating from the lower gastrointestinal
tract.

Melena

Black, tar-like, sticky stools that originate
from bleeding of the upper gastrointestinal
tract

Hematuria

Red blood cells in the urine

Hemoptysis

Coughing up blood (originates from the
airway)

Menorrhagia

Heavy menstrual bleeding

Epistaxis

Bloody nose

Purpura v petechia

Small, flat spots beneath the skin or mucous membranes indicative of bleeding.
They range in color (purple, red, or brown depending on the skin tone)
purpura - larger, blobbier
petechia - fine pinpoint spots

Extrinsic and
Common Pathway Lab tests

PT (Prothrombin Time)
INR (International Normalized
Ratio) - Measures how long it
takes for a patient's body
to form a clot

Intrinsic pathway lab tests

APTT (Activated Partial
Thromboplastin Time) - Measures how long it
takes for the blood to form
a clot

causes of decreased platelets

Chemotherapy, radiation, cancer of the bone marrow (platelets are produced in the bone marrow, cancer can
cause a low platelet count)
• B12/folate deficiency (associated with low platelet counts)
• Medications (Thiazides, Digoxin, Heparin - all of these can reduce platelet count)
• Splenic sequestration (spleen enlarges and functions abnormally, decreases platelet count in circulation)
• Large blood transfusions (dilutes platelet count)

Thrombocytopenia

Abnormally low platelet levels, symptoms present when count falls below ~100,000 - Easy bruising, mucosal hemorrhage, petechiae, purpura,
"deep" bleeding beneath the tissues

Idiopathic
Thrombocytopenic
Purpura (ITP)

Immune-mediated destruction of platelets, can be triggered by an acute viral infection or autoimmune diseases (e.g. AIDS, Lupus) - Easy bruising, bleeding beneath the skin (purpura –
appears like a rash), bleeding from mucosa, blood in urine or stools, heavy menstrual flow

Heparin-InducedThrombocytopenia (HIT)

A serious complication of taking the anticoagulant
Heparin. The immune system causes the platelets to clot in the presence of Heparin, causing the platelet levels to reduce. - Pain, swelling, redness, or tenderness in one or several extremities (blood clot), hypertension, tachycardia, chest pain (pulmonary embolism)

Hemophilia A (X-Linked disorder)

Clotting Factory VIII (8) deficiency Most common (85% of cases) - Spontaneous bleeding of the joints, mucosa, GI tract, and brain (intracranial)
Prolonged bleeding after minor procedures (e.g. dental)

Hemophilia B (X-Linked disorder)

Factor IX (9) Deficiency "Christmas Disease" - Spontaneous bleeding of the joints, mucosa, GI tract, and brain (intracranial) Prolonged bleeding after minor procedures (e.g. dental)

DIC (Disseminated Intravascular Coagulation)

A rare blood clotting disorder that can cause organ damage and uncontrollable bleeding Can be activated from sepsis or massive trauma. - Uncontrollable bleeding from various parts of the body, such as the nose and mouth. Decrease blood pressure, blood clots, bruising, confusion. "Death Is Coming"

Hepatic Disease

Chronic liver disease that causes decreased
synthesis of clotting and inhibitor factors - Due to reduced clotting and inhibitor factors, the patient will have a perceived "hypo coagulable state", having prolonged bleeding tendencies

Vitamin K Disorder

Infancy: Babies need Vitamin K supplements as their gut cannot make enough (associated with low vitamin K levels in their formula or breast milk)
Acquired: Attributed to malnutrition, malabsorption (biliary disease), antibiotic therapy, anticoagulation therapy

Hemoglobin

Hemoglobin made of two alpha and two beta chains. Can carry 4 oxygen.
Infant: Two α (alpha) chains and two γ (gamma/fetal) chains
• Gamma chains are the primary hemoglobin in a developing fetus
▪ A more efficient oxygen carrier under conditions of decreased oxygen
tension
• At birth, gamma chains deplete, and as the fetus develops, they form beta
chains
• Adulthood: Two α (alpha) chains and two β (beta) chains
• 97-98% of adult hemoglobin consists two alpha and two beta chains
• 2-3% of adult hemoglobin consists of two alpha and two delta (δ) chains

Erythropoiesis

It is the production of red blood cells (RBCs), which occurs in the bone marrow.
• A hormone known as erythropoietin (EPO) triggers red blood cell production
o EPO is secreted by the kidneys
Erythropoiesis Feedback Circuit
Not Enough RBCs in Circulation:
• Tissues lack oxygen due to low RBCs - Kidneys secrete EPO - EPO stimulates bone marrow
to make more RBCs
Too many RBCs Circulation:
• Kidneys detect an increase in hemoglobin - Kidneys secrete less EPO - Bone marrow
makes less RBCs
o Homeostasis is achieved

RBC indices

Three Components:
• MCHC: Mean Corpuscular Hemoglobin Concentration
o The concentration of hemoglobin in red blood cells
• MCH: Mean Corpuscular Hemoglobin
o The average amount of hemoglobin in a red blood cell
• MCV: Mean Corpuscular Volume
o The overall size of the cell
o Three Types: Normal (Normocytic), Big (Macrocytic), Small (Microcytic)

For the exam, consider MCH/MCV going hand in hand with representing the size of RBCs
• Consider MCHC as what represents the color of the RBCs (normal/pale)

Iron Deficiency Anemia

Low iron, which is important to make hemoglobin
Iron can be lost most commonly due to GI bleeds
in men, and menorrhagia in women
Low MCV, MCH, MCHCH
RBC indices: hypo chromic, microcytic

B12/Folate Deficiency

Not enough RBCs are produced due to a deficiency in B12 (pernicious anemia) and/or folate.
A deficiency in B12 may result from low intrinsic
factor.
High MCV, High MCH, normal MCHCH
Macrocytic, normal hemoglobin levels
Forms big RBCs called megaloblasts,
which cannot divide and reproduce like
healthy RBCs

Anemia due to Chronic Kidney Disease

Chronic Kidney Disease shuts off the oxygen
sensor, inhibiting the ability to release EPO (Less
RBC production)
Normal MCV, MCH, MCHCH
Burr Cells (unique to Chronic Kidney
Disease - oddly shaped, spikey)
Normal RBC indices - size of cell and
amount of hemoglobin doesn't change)

Thalassemia

Genetic mutations that result in deficient synthesis
of globulin chains (hemoglobin deficiency) Clinical presentation can range from asymptomatic to hydrops fetalis (collection of fluid in unborn or
newborn babies)
Low MCV, MCH, MCHCH
Hypochromic, microcytic cells

Acute Blood Loss

Trauma that results in acute blood loss and
eventually anemia
normal MCV, MCH, MCHCH
Red blood cells are normal, there is
just a reduced quantity in circulation

oxygen hemoglobin dissociation curve

Shift to the Right (Reduced Affinity – allows more oxygen to be available to the tissues)
• More oxygen is needed, the bind between oxygen and hemoglobin decreases
o Increased CO2
o Increased temperature
o Lower pH (acidotic)
Shift to the Left (More Affinity - less oxygen available to the tissues)
• Less oxygen is needed, causing the bind between oxygen and hemoglobin to increase
o Decreased CO2
o Decreased temperature
o Higher pH (alkalotic)

Ventilation

The mechanical movement of
air (breathing)

Conduction

The part of the respiratory
tract that moves air in and out of the lungs

Respiration

The physiologic gas exchange
in the alveoli (oxygen and carbon dioxide
exchange)

Circulation

The bloodstream takes in
oxygen to deliver to the tissues and carries
carbon dioxide to the lungs to be excreted
through exhalation

Ventilation/Perfusion (V/Q) Matching

A ratio that describes the relationship between the amount of air reaching
the alveoli (ventilation) and the flow of blood in the surrounding capillaries
for gas exchange (perfusion)
● An optimal ratio ensures oxygen is efficiently entering the lungs and
being transferred to the bloodstream, as well as the removal of carbon
dioxide

Low V/Q

Alveoli are poorly ventilated but adequately perfused
○ Hypoxia

High V/Q

Alveoli are adequately ventilated but poorly perfused
○ Hypercapnia

AA gradient

Measures the difference between the oxygen concentration in the alveoli and arteries
● PAO2 (oxygen in alveolus) - PaO2 (oxygen in the arteries = AA gradient
○ Typically < 10mmHg
○ Helps us identify difficulties in gas exchange
○ Widening of the gradient indicates worsening lung function

Tidal volume

The volume of air that enters and exits the lungs
with each breath (normal)

Inspiratory reserve volume

Additional volume that can be
inspired above tidal volume (deep inhale)

expiratory reserve volume

Additional volume that can be
expired tidal volume (deep exhale)

Residual volume

Volume of air remaining in the lungs following
maximum expiration

vital capacity

Volume of air that can be exhaled after maximum
inspiration

inspiratory capacity

Volume breathed in from normal expiration
to deep inspiration

functional residue capacity

Volume remaining after normal
expiration

total lung capacity

Volume of air in lungs after maximum
inspiration

Acute Respiratory Distress

Inflammation within the lungs impairs alveoli from filling with
air, acutely impairing gas exchange
Patients experience an abrupt increase in breathing
(accessory muscle use, tripoding, tachypnea, speaking in
shorter sentences)
● Compensating for a lack of oxygen in the bloodstream
● Lack of impairment to mental status, circulation

Acute Respiratory Failure

The lungs cannot exchange oxygen and carbon dioxide
properly.
● Causes: Drugs (opioids), asthma (closing of airways),
chronic lung diseases (e.g. COPD), infectious illness (e.g.
sepsis)
● ABG: PaO2 < 60 mmHg (not enough oxygen), PaCO2 >
50mmHg (too much CO2 in the blood)
● Clinical Manifestations: Rapid, shallow breathing that
declines to slow, irregular breathing (tires out), accessory
muscle use, mental status changes (lack of oxygen),
cyanosis

pulmonary embolism

A clot from another location in the body (for example, a deep vein
thrombosis in the lower extremities) travels to an artery in the
lung and obstructs blood flow.
● Clinical Manifestations: Sudden onset of chest pain, dyspnea
(difficulty breathing), hemoptysis (coughing up blood),
tachycardia, tachypnea
● Virchow's Triad: Venous stasis (clots form when blood pools),
hypercoagulability (cancer, pregnancy), intimal/vessel wall
injury (trauma)

FEV1/FVC Ratio

Indicates how much air you can forcefully exhale. A normal ratio is
typically 0.75 - 0.80.

Obstructive respiratory disease

Difficulty moving air out of
the lungs (COPD, Asthma)
FEV1 / FVC ratio < 75%

restrictive respiratory disease

Difficulty moving air into the lungs (interstitial
fibrosis, granulomatous disease, pneumoconiosis,
scleroderma (collagen diseases), neuromuscular
diseases
FEV1 / FVC ratio normal (equally reduced)

Cystic fibrosis

Bronchiolitis

Inflammation of the bronchioles; viral
Common in young children (2 and younger)

Wheezing, dyspnea, tachypnea, low grade fever

Epiglottitis

Inflammation of epiglottis; bacterial
Uncommon due to vaccinations
Swollen, red throat, drooling, dysphagia, fever, stridor

Croup

Common in children 6 months – 3yrs
Viral or bacterial
Barking cough, stridor, low-grade fever

ARDS
acute respiratory distress syndrome

Etiologies include aspiration, shock, sepsis, trauma; mechanism unknown
Refractory hypoxemia, non-cardiogenic pulmonary
edema

IRDS (hyaline membrane disease)

Pre-term infants (<25 weeks – NICU)
Immature lungs, lack of surfactant decrease
compliance
Respiratory distress, intercostal retractions, nasal flaring

URI (upper respiratory tract infection)

Sinusitis (usually viral or allergic)
Runny nose, sneezing, watering of the eyes

LRI (lower respiratory tract infection)

Bronchitis – often viral, pneumonia

pneumonia

Etiology: Inhalation of an infectious agent, aspiration, systemic disease
Community Acquired vs Nosocomial
● Community Acquired:
○ Bacterial: fever/chills, "wet cough"
○ Viral: "dry cough"
○ Atypical: "Walking Pneumonia" - Slower onset of symptoms, high fever, GI symptoms, muscle pain
● Nosocomial (Hospital-Acquired): Opportunistic (immunocompromised), ventilator-associated
pneumonia

Tuberculosis

Primary: Can be asymptomatic for years
Reactivated: Fever, cough, night sweats, weight loss

Body fluid distribution

2/3 is intracellular
○ Potassium (K+) is the most prevalent ion in intracellular fluids
○ Potassium is the most commonly affected ion during acid-base imbalances
● 1/3 is extracellular
○ Sodium (Na) is the most prevalent ion in extracellular fluids

capillary pressures

Hydrostatic Pressure: Drives fluid out of the vasculature
Oncotic Pressure: Pulls fluid into the vasculature

Respiratory acidosis

Low pH, high CO2 due to decreased respirations
(retention of CO2 – which is acidic and can lower pH)
Causes: Opioids, COPD, Asthma, Chest injury

Respiratory alkalosis

High pH, low CO2 due to excessive respirations
(rapidly excreting CO2, raising the pH)
Causes: Hyperventilation (e.g. anxiety)

Metabolic acidosis

Low pH, low HCO3 due to an increase in
acidity/decrease in bicarbonate ions (alkalotic –
increases pH)
Causes: DKA, severe infection, toxin ingestion,
burns

metabolic alkalosis

High pH, high HCO3 due to increase in bicarbonate
(alkalotic, increases pH)
Causes: Vomiting (loss of stomach acid), intake of
bicarbonate (antiacids)

hyponatremia

(low sodium
Cells have a water excess – dilutes
amount of sodium in the cells
Causes: Water poisoning, SIADH,
replacement of fluids without salt

hypernatremia

(high sodium)
Cells are deficient in water – concentrates
amount of sodium in the cells
Causes: DI, prolonged vomiting/diarrhea,
diaphoresis

hypokalemia

(low potassium)
Decreased potassium in cells
Causes: Diarrhea, vomiting, potassium-
wasting diuretics, excess insulin

hyperkalemia

(high potassium)
Increased potassium in cells
Causes: IV potassium, insufficient insulin,
aldosterone-inhibitors (decreases extretion
of potassium)

hypocalcemia

Decreased calcium in cells
Causes: Vitamin D deficiency, dietary
insufficiency
Can cause muscle spasms/twitching

hypercalcemia

Increased calcium in cells
Causes: Vitamin D excess, cancer (multiple
myeloma)
Can cause muscle weakness

vasculature anatomy

Arteries: Thicker walls than veins (can
withstand higher pressures), carries
oxygenated blood to the heart
● More prone to atherosclerosis
Veins: Thinner walls than arteries,
carries deoxygenated blood to the heart
When vessels dilate (widen), blood
pressure decreases
When vessels contract (get smaller),
blood pressure increases

vascular insufficiency - arterial pain

Claudation (pain with
movement), painful
ulcers

vascular insufficiency - arterial skin manifestations

Cool,
decreased/absence of
hair, pallor, diminished
pulses

vascular insufficiency - venous pain

Aching/cramping, ulcers
(not as painful as arterial)

vascular insufficiency - venous skin manifestations

Warm, reddish/brown
pigmented areas, varicose
veins

abdominal aortic aneurysm

A bulge in the wall of the aorta that
can rupture.
Patients describe it as a sudden
onset of severe chest pain
● Ripping, tearing quality that
can radiate to the back

Mean arterial pressure (MAP)

The average pressure within the circulatory system
● Calculation: (2 x Diastolic) + Systolic / 3
● Indicative of how well blood is circulating throughout your body and perfusing vital organs

pulse pressure

Represents the force the heart generates each time it contracts
● Calculation: Systolic Pressure – Diastolic Pressure
○ A higher pulse pressure means the heart is working harder
○ A narrow pulse pressure means the heart isn't pumping enough blood

hypertension

Elevated blood pressure
• Essential (Primary) Hypertension: 90% of cases, attributed to obesity, family history, diet,
exercise habits (not due to a medical condition)
• Secondary Hypertension: Elevated blood pressure due to a medical condition (renal disease,
malignant hypertension, adrenal tumor, medications, etc.)

End organ damage

Severe impairment of major organs due to high blood pressure
• Heart, Kidney, Brain, Eyes

shock

A life-threatening condition when there is insufficient blood flow to the organs and
tissues
Adequate perfusion of the body is measured with a patient's blood pressure
● BP = HR x SV x SVR
○ HR: The amount of times the heart beats per minute
○ SV: Stroke volume (volume of blood put out with each heart beat)
○ HR x SV = Cardiac Output (volume of blood put out each minute)
○ SVR: Systemic Vascular Resistance (size of vessels)
Note: Nitrous oxide can cause further hypotension, which can be dangerous

compensated shock stage

pulse rate increases
respirations increase
weak pulse
cool, clammy skin
anxious, restless, combative
thirsty, weak

decompensated shock stage

very weak or absent pulse
severe drop in BP
altered mental status/unconsciousness
slow breathing/apnea

irreversible shock stage

cell death
organ system failure
washout
hemorrhaging all over
death

cardiogenic shock

The heart is unable to
adequately pump enough blood
to the body
caused by Myocardial infarction,
Cardiomyopathy, Valvular
dysfunction
HR, SV affected

obstructive shock

Blockage or compression of the
heart's vessels, decreasing
cardiac output
caused by Pulmonary embolism (sudden
chest pain, dyspnea), Cardiac
tamponade (fluid in the
pericardial sac), Tension
pneumothorax (heart and
contralateral lung compressed)
SV affected

hypovolemic shock

Insufficient blood volume or
extracellular fluid in the body
caused by Hemorrhage, dehydration
SV affected

distributive shock

Abnormal distribution of blood
flow results in inadequate blood
supply to tissue/organs
caused by Anaphylactic, neurogenic (brain
trauma, spinal injury), sepsis
SVR affected

shock complications

ARDS, DIC, acute renal failure, MODS (multiple organ dysfunction system)