Cardiology: Shock and Ischemia

Shock caused by inadequate function of the heart, or pump failure.

Ischemia-induced myocardial chest pain caused by spasms of the coronary arteries

inflammation of endothelium that lines heart and cardiac valves. most commonly damages mitral valve, then aortic and tricuspid valves. commonly caused by bacteria that are normally present in the body. can also occur after an invasive medical or dental procedure. symptoms: valvular dysfunction, may affect organ systems, chest pain, CHF, clubbing, meningitis, low back pain, arthralgia, arthritis

streptoccal infection causes damage to heart valves

Mitral valve stenosis
Mitral valve regurgitation
Mitral valve prolapse

Aortic valve stenosis
Aortic valve regurgitation

inflammation of the pericardium

acute compression of the heart caused by fluid accumulation in the pericardial cavity

disease of the heart muscle

congenital malformation involving four distinct heart defects

(inflammation of blood vessles, hence the strawberry tongue) causes coronary artery aneurysms.

a chronic condition in which the heart is unable to pump out all of the blood that it receives

dia- RV - dont accept enough blood
sys- RV - cant pump enough blood to lungs

irregular heartbeat

LV: dyspnea, dulled mental status, decreased urine output

RV: abdominal discomfort, peripheral edema, unexpected overnight weight gain, JVD

anxiety

falling O2 sat

tachycardia w/ weak pulse

hypotension

S3 systolic dysfunction, S4 diastolic dysfunction

shock resulting from blood or fluid loss

redness, heat, swelling, pain

Swelling, heat, ache, redness, pain

loss of function

pump

coronary artery disease

coronary artieries

repeat injury to the endothelium

condition in which fatty deposits called plaque build up on the inner walls of the arteries

A build up of cholesterol along the walls of arteries (fatty material)

chest pain that results when the heart does not get enough oxygen

acute coronary syndrome

chest pain that occurs when a person is active or under severe stress

chest pain that occurs while a person is at rest and not exerting himself

a condition in which blood flow to part of the heart muscle is blocked, causing heart cells to die

blood clot

A clot that breaks lose and travels through the bloodstream.

pulmonary edma

1-Superior & Inferior Vena Cava, 2-Rt Atrium, 3-Tricuspid Valve, 4- Rt Ventricle, 5-Pulmonary Valve, 6-Pulmonary Artery, 7- Lungs-pick up oxygen, 8-Pulmonary Veins, 9- Lt Atrium, 10- Mitral Valve (Bicuspid), 11-Lt Ventricle, 12- Aortic Valve, 13-Aorta, 14- Body

Tunica externa: collagen fibers (outmost)
Tunica media: smooth muscle & elastin
Tunica intima: endothelium (innermost)

tunica media
rational: the tunica media is composed of smooth muscle which can stretch, expand to accommodate changes in blood pressure

Food and O2 pass into tissues
Wastes and CO2 pass from tissues into blood
Creates compounds that stimulate
vasodilation or vasoconstriction
stimulate smooth muscle
promote clot formation in injured area
inflammation

protein and fat clusters that transport fats in the blood

low-density lipoproteins "the bad cholesterol"
- Lower density: less protein, more cholesterol
- Transports cholesterol from the liver to cells
- Can be oxidized and deposited

high-density lipoproteins "the good cholesterol"
- Higher density: more protein, less cholesterol
- Transports cholesterol from cells to the liver
ldl is considered to be good cholesterol

false

accumulation of lipoproteins within the walls of an artery

Monocytes attach to the endothelium → macrophages
.• Macrophages release free radicals (damaging to endothelium) → oxidized LDL.
• Macrophages ingest oxidized LDL → foam cells
.• WBCs, platelets, and vascular endothelium releasechemicals that promote plaque formation
.• Plaques block the arteries

A plaque that has a large lipid core and a thin cap, and can rupture more readily, producing a thrombus. Involved in acute coronary syndromes

clots may break loose and block blood flow to key organs

Peripheral Arterial Disease (PAD)—atherosclerotic blockages
− Large arteries (not coronary, aortic arch, brain)

• Thromboangiitis Obliterans (Buerger's disease)—nonatherosclerotic inflammation and thrombosis
− Small- and medium-sized arteries and veins

• Raynaud Phenomenon—intense vasospasm
− Arteries, arterioles in the fingers and toes

supply oxygen-rich blood to the myocardium
runs on the outside of the heart

hardening of the arteries

strangle

ok at rest but chest pain during activity
heart low on oxygyen

Elastin and collagen fibers
Water content
Surface tension

Amount of air that moves in and out of the lungs during a normal breath

Common cold
Rhinosinusitis
Influenza

Occur in early fall and late spring in person between ages 5 and 40

occur in children younger than 3

Occur in winter and spring in children younger than 3

Occur in winter and spring

sinus drainage

facial pain, headache, purulent nasal discharge, decreased sense of smell, fever

nasal obstruction, fullness in the ears, postnasal drip, hoarseness, chronic cough, loss of taste and smell, unpleasant breath, headache

like a common cold with profound malaise

Fever, tachypnea, tachycardia, cyanosis,hypotension

three or more particles) ordirect contact.

Inflammation of Alveoli and Bronchioles

Bacteria in the Alveoli
Lobar: affects an entire lobe of the lung
Bronchopneumonia: patchy distribution over more than one lobe

Viral and mycoplasma infections of the alveolar septum or interstitium

World's foremost cause of death from a single infectious agent•
Causes 26% of avoidable deaths in developing countries
• Drug-resistant forms
• Mycobacterium tuberculosis hominis
- Aerobic- Protective waxy capsule
- Can stay alive in "suspended animation" foryears

Hematologic or lymphatic dissemination of TB

grains of millet in the tissues

Meat inspectionwas introducedto keep them outof the foodsupply
.• Pasteurization ofmilk wasintroduced tokeep TB out ofthe milk supply

Signs of pneumonia
- Bacteria in sputum and exhaled droplets
- Bacteria may erode blood vessels and spread through the body
=miliary tb

Reinfection from inhaled droplet nuclei
• Reactivation of a previously healed primarylesion
• Immediate cell-mediated response walls off infectionin airways
• "Consumption": eventually fatal if untreated

Secondary
Rationale: Secondary TB, often referred to as reactivation or reinfection TB.• may occur if patients are re exposed to TB bacilli (after a primary infection) or if they become immunocompromised (they are unable to contain the infection).

epithelial cells lining the lungs

Large cell carcinomaº
Squamous cellº
Adenocarcinoma

Small cell and non-small cell

nuclues and cell wall are close to eachother
typically in female with long history of smoking
divides quickly and spreads rapidly
accure 15 percent

-alot of distance from nucleus to cell wall
-secretes mucin, responsible for keeping lungs moist
-adenocarcinoma = adeno means gland
occurs 40 percent affects smokers and non
-squmous call carcinoma, two cells become cancerous
occurs 30 percent men greatest link to smoking
-large cell carcinoma, ocurrs in 10 percent of male smokers

Lack of surfactant;infants are not strong enough to inflate their alveoli.

True
Rationale: in RDS occurs due to a lack of surfactant the alveoli (the surfactant is produced by alveolar cells and keeps them inflated).

croup,
epiglottitis
Croup- "bark-likecough"- Epiglottitis-infection

Acute bronchiolitis

True
Rationale: Epiglottitis affects the upper airway (inflammation causes the lumen of the upper airway to become more narrow).When the child inspires, it is difficult to pass air through then arrowed airway. This causes noisy inspiration/stridor.

disease of the lung that causes a decrease in lung expansion. becomes hardend
inspiratation problem
ex fibrosis/scar tissue
chest wall like muscluar dieases
amyloidosis are protein particles that get stuck in the lungs

disease with increase resistance
exhale problem
air is trapped in the lungs by clot or walls narrowing from lost of elasticity
large over inflated lungs
ex COPD= emphysema lungs losing it elsastic quality and Chronic Chroncitis is alot of irritation and mucus
asthma air way spasm and closes up blocking air from exiting

An inflammation of lung tissue, wherer the alveoli in the affected areas fill w/fluid and oxygen and c02 builds up and more c02 in the body

fluid where its not suppsed to be or to much

clot in the lungs that stops the gas air exchange from happening

lines the thoracic wall and superior aspect of the diaphragm

covers the lungs

or the space between the two layers contains a thin layer of serous fluid.

Hydrothorax: serous fluid
Empyema: pus
Chylothorax: lymph
Hemothorax: blood

air in the pleural cavity
Air takes up space, restricting lung expansion.
• Partial or complete collapse of the affected lung:- -Spontaneous: air-filled blister on the lung ruptures- -Traumatic: air enters through chest injuriesº
-Tension: air enters pleural cavity through wound on inhalation, cannot leave on exhalationº
Open: air enters pleural cavity through the wound on inhalation and leaves on exhalation

False
Rationale: In Open Pneumo thorax, inhaled air compresses the affected side's lung, but during exhalation, the lung reinflates somewhat.In Tension Pneumothorax, a sort of one-way valve exists—the air enters the affected side during inhalation,but is unable to leave when the patient exhales.Therefore, all of this air exerts increased pressure on the organs of the thoracic cage. Unless the pressure is relieved, tension pneumothorax is fatal*

Rationale:

Prostaglandins and leukotrienes cause vasodilation, which brings more blood to the injured/affected area. The symptoms caused by this vasodilation are redness/erythema and warmth.

Circulate in the blood in an inactive form → highly toxic proteins → destroy antigen

Cells and fluid that have seeped out of blood vessels or an organ, especially with inflammation

Serous- clear, thin fluid
.• Hemorrhagic-RBCs.
• Fibrinous- fibrin. tissue injury typically
.• Membranous, pseudomembranous-mucous membrane surfaces.
• Purulent, suppurative- thick/viscous/opaque. pus

False
Rationale: The surface epithelial cells of the skin are most likely to be damaged in this instance. Surface epithelial tissue has the ability to regenerate, replacing the damaged tissue with the same type (epithelial).

Local responses→ Vascular stage→ Cellular stage

Systemic (whole-body) responses→ White blood cell response→ Acute-phase response

WBC count rises → leukocytosis.
• Immature neutrophils released into blood.

True
Rationale: When the body senses a change out of the norm, it activates mechanisms that oppose that change(vasodilation and sweating with increased temperatures;vasoconstriction and shivering with decreased temperatures). This is known as negative feedback.
Positive feedback, on the other hand, senses a change but activates a mechanism that exaggerates the change

Always present
• Attacks nonself microbes
• Does not distinguish between different microbes• Mechanisms include:- Epithelial barrier
- Phagocytic cells- Plasma proteins- Cell messenger molecules

Attacks specific microbes (antigens)
• Develops after exposure to specific antigen
• Mechanisms include:- Humoral immunity - Antibodies from Bcells/lymphocytes- Cell-mediated immunity - Tcells/lymphocytes

True
Rationale: In adaptive/acquired immunity, specific antigens are attacked, and immunity develops after exposure to the specific antigen.When you get a vaccine, you are getting a live,weakened, or dead microbe (a specific antigen).Your body develops antibodies to attack that antigen after you are exposed

control immune response

then carry out the attack on antigen

Chemokines: Cytokines that attract WBCs to the infection- Colony-Stimulating Factors (CSFs): stimulate WBCs to divide and mature

Circulate in the blood in an inactive form → highly toxic proteins → destroy antigen

genes that code for cell surface proteins essential for the acquired immune system to recognize foreign molecules, which in turn determines histocompatibility.

t helper

t cyctotoxic

→ Plasma cells secrete antibodies.
→ Memory B cells remain in the body for subsequent, quicker reactions.
IgG: circulates in body fluids, binding antigens
.• IgA: found in secretions on mucous membranes;prevents antigens from entering the body.
• IgM: circulates in body fluids; has five units to pull antigens together into clumps

Lymphocytes
Rationale: Remember that antibodies are created in response to antigens. B lymphocytes have antigen receptors and are activated to produce antibodie against that antigen if a T helper cell directs them to do o

False
Rationale:In active immunity, an individual is exposed to anantigen, the immune response begins, and antibodies areformed in 7 to 10 days.In passive immunity, antibodies are created outside the
host and injected, giving the individual immunity
immediately.

Excessive or inappropriate activation of the immune response
The body is damaged by the immune response, rather than by the antigen

Commonly called "allergic reactions"
• Systemic or anaphylactic reactions
• Local or atopic reactions (genetic)- Urticaria (hives)- Rhinitis (hay fever)- Atopic dermatitis- Bronchial asthma
• Food allergies

True
Rationale: Histamine is one of the first chemical mediatorsreleased during the inflammatory response as a result ofmast cell degranulation. Mast cell stabilizers (used totreat asthma) prevent the histamine from beingreleased; antihistamines (used to treat allergies)compete with histamine for receptor sites, lessening theinflammatory response.

vasodilation.

• Complement- and antibody-mediated cell destruction,inflammation, cell dysfunction
• IgG or IgM binds antigens on cell surfaces

It has neither A or B antigens on the RBC.
Rationale: Antigens are the components that elicit animmune response (type II hypersensitivity reaction).Type O blood does not have AB antigens on the RBC, so anyone can receive it because there is nothing to stimulate production of anti-A or anti-B antibodies against it. The fact that type O blood has both A and B antibodies has nothing to do with creating the antigen-antibody response.

immune complexes deposit on walls of blood vessel sand activate complement → damaged blood vessels• Systemic- Autoimmune vasculitis, glomerulonephritis, serumsickness (antibiotics, food, venom