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Patho: pulmonary; cardi; hemo; GI; Urinary > Patho Final > Flashcards

Patho Final Flashcards

1
Q 
Cell Biology:
Altered tissue changes:
Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia
A
  • Atrophy
  • Hypertrophy
  • Hyperplasia: an increase in the reproduction rate of organ cells
  • Metaplasia: is the transformation of one differentiated cell type to another differentiated cell type
  • Dysplasia: abnormal growth or development of cells
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2
Q

Cancer:

Benign/ Malignant

A

-Benign: usually well encapsulated, does not invade or spread to distant locations.
Considered “relatively innocent,” implying that it will remain localized, is generally amenable to local surgical removal, and patients generally survive.

-Malignant: rapid growth rates; lack of capsule; invasion into blood vessels, lymphatics, and surrounding structures; and distant spread.

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3
Q

Cancer:

Characterization of cells/ tumors

A

-Benign: suffix – oma

-Malignant: From epithelial cell origins are called “carcinomas”
From non-epithelial tissue origins are called sarcomas

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4
Q

Immune System:

Inflammation process

A

SHARP= Swelling, Heat, A loss of function, Redness, Pain (nonspecific)
1) An antigen finds its way into the ISF; chemokines “help!” neutrophils first responder

2) Mast cells: chemotactic factors; release histamine- causing vasodilation; prostaglandins- causing pain
3) Phagocytosis: ~24hr macrophages and dendritic cells; APC to T and B cells
4) Plasma Protein System: complement system- things tagged to be destroyed; coagulation system- clotting; Brady Kinin- dilation, pain (the inflammatory response)

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5
Q

Immune System:
HIV
AIDS

A

-HIV: infects and destroys Th cells, which are necessary for the development of both B cells (humoral immunity) and cytotoxic T cells (cellular immunity).

AIDS- Th cells <200 cells/mm3; the most advanced stage of HIV infection.

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6
Q

Neurological:

Pain pathway

A

1) Transduction: Tissue damage; activates Brady Kinin/ prostaglandins; they activate pain; activation of action potential; release of nociceptors (large A/ small C)
2) Transmission: nociception sent via large A/ small C; to spinal cord; brain stem; thalamus; cortex of brain
3) Perception: awareness of pain
4) Modulation: endorphins from brain stem bind to opioid receptors to inhibit pain impulse

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7
Q

Neurological:

CVA

A

1) Ischemia: blood flow is blocked to part of the brain causing hypoxia then ischemia.
- Thrombotic: Clot forms in the brain blocking blood flow. Athlero.
- Embolic: Fragments that break from a thrombus formed outside the brain but then travels to the brain and blocks blood flow.
- Transient ischemic attacks (TIAs): Results from ischemic event. Neurological dysfunction lasting <1 hour.
- Associated with systemic hypoperfusion resulting in inadequate blood supply to brain

2) Hemorrhagic: Bleeding causes compressed brain tissue, leading to ischemia, edema, and increased ICP and necrosis
- May be a result from a ruptured aneurysm.
- HTN is the primary cause.

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8
Q

Fluid/ Electrolyte/ pH:

3 Main electrolytes and their imbalances

A

1) Sodium:
2) Potassium: resting potential
3) Chloride: threshold potenital

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9
Q 
Fluid/ Electrolyte/ pH:
Buffering Systems (3)
A

1) Carbonic Acid-Bicarbonate Buffering (blood buffer):
cellular respiration creates CO2, which combines with water to form H2CO3. H2CO3 dissociates, forming one hydrogen (H+) ion and one bicarbonate ion (HCO3). These reactions are readily reversible, depending on whether an acid or a base environment exists.

2) Lungs: though CO2 regulation.
increase CO2 excretion = increase pH= BASIC (hyperventilation)
decrease CO2 excretion = decrease pH ACID (Dyspna)

3) Renal Buffering: reabsorbing or regenerating bicarbonate in the renal tubules or excreting hydrogen into the urine.
increase H+ excretion= increase pH (BASE)
increase HCO-3 excretion = decrease pH (ACID)
**actually gets rid of what we don’t want

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10
Q

Fluid/ Electrolyte/ pH: Main electrolytes and their imbalances
Sodium
s/s

A

1) Sodium: ECF
-Hypernatremia= Hypretonic solution (Na+ out of cell)
Intracellular dehydration: thirst (cells want to return to an isotonic state), weakness, HTN
-Hyponatremia= Hypotonic Solution (Na+ into cell)
Headache, nausea, hypotension, muscle cramps, seizures; cerebral edema and ICP leading to coma (fatal)

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11
Q

Fluid/ Electrolyte/ pH: Main electrolytes and their imbalances
Calcium
s/s

A

2) Calcium: ICF
Hypercalcemia= decrease skeletal muscle excitability (muscle weakness, fatigue/lethargy, kidney stones, constipation)
increase Threshold potential = Less excitable causing weakness
-Hypocalcemia= increase neuromuscular excitability (muscle cramps/spasms, intestinal cramping)
decrease threshold potential = More excitable causing muscle cramping

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12
Q

Fluid/ Electrolyte/ pH: Main electrolytes and their imbalances
Potassium

A

3) Potassium: ICF
- Hyperkalemia= Acidosis (H+ moves INTO the cell). Increase resting potential increase cardiac excitability; tingling, restlessness, intestinal cramps/diarrhea, cardiac dysrythmias.
- Hypokalemia= Alkalosis (K+ moves INTO the cell). Decrease resting potential decreased cardiac excitability; skeletal muscle weakness, smooth muscle atony, and cardiac dysrhythmias

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13
Q

Fluid/ Electrolyte/ pH:

4 Main pressures/ forces involved in fluid balance

A

1) Capillary Hydrostatic Pressure: strongest pressure; blood pressure = push of fluid out of capillary
2) Capillary Oncotic Pressure: water attraction to albumin = pull of fluid into capillary
3) Interstitial Hydrostatic Pressure: Interstitial fluid pressure = Push of fluid out of tissues
4) Interstitial Oncotic/ Osmotic Pressure: weakest pressure; water attraction to interstitial proteins/electrolytes= pull of fluid into capillary

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14
Q 
Pulmonary: Pneumothorax 
Open
Tension
Spontaneous
Secondary
A

Pneumothorax: whole lung collapses, disrupting the negative air pressure surrounding the lung

1) Open pneumothorax: spontaneous or secondary- hole in lung through visceral and parietal. Pressure now = Pb pressure (barometric).
2) Tension pneumothorax: tear in the visceral OR parietal and trapped in the pleura cavity (air enters but cannot leave). Pip becomes > Pb
3) Spontaneous pneumothorax: random spontaneous rupture or tearing of visceral layer (inside)
4) Secondary pneumothorax: rupture or tearing of parietal layer (outside) or visceral layer (inside) due to something external tearing

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15
Q

Pulmonary: COPD

Asthma

A 
Chronic inflammatory disorder of the airways
Hypersensitivity induced (typically type 1)

Inflammation results from hyper-responsiveness of the airways

Can lead to obstruction and status asthmaticus
Expiratory wheezing, dyspnea, and tachypnea

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16
Q

Pulmonary: COPD

Emphysema

A

Related with smoking and genetics

Abnormal permanent enlargement of the gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis
Loss of gas exchange for surface area

Loss of elastic recoil- have a hard time exhaling

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17
Q

Cardiovascular:

BP and how it is measured

A

BP = cardiac output X peripheral resistance

BP: force forward and against the vessel wall
CO: amount of blood ejected per min
PR: the overall amount of RESISTANCE in the body (vasodilation/ vasoconstriction)

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18
Q

Cardiovascular:

Most common type of HTN and its cause

A

Primary Hypertension: BP > 140/90 mm Hg

  • Essential or idiopathic (don’t know what is causing it) hypertension
  • Genetic (African American)
  • Environmental factors (diet, Na+ intake)

Affects 92% to 95% of individuals with hypertension

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19
Q

Cardiovascular:

Left heart failure

A

blood ejection to the systemic system (most common)= Congestive HF
Blood backs up in pulmonary veins (lungs)

PULMONARY HTN
-cyanosis, cough, crackles, wheezing, PE- frothy bloody sputum, S3/ S4

MVP is most common reason

Hypertrophied
Overly compliant

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20
Q

Cardiovascular:

Right heart failure

A

Most commonly caused by a diffuse hypoxic pulmonary disease (COPD/ARDS)- vasoconstriction due to shunting
Backed up into systemic vessel

SYSTEMIC HTN
-JVD, dependent edema, increase peripheral venous pressure, ascites

Also caused by left vent. failure
Can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation

21
Q

Cardiovascular: Coronary Artery Disease (CAD)
Cause
Effect
s/s

A

Any vascular disorder that narrows or occludes the coronary arteries causing ischemia then infarction
-Atherosclerosis is the most common cause

-Myocardial ischemia
Local deprivation of the coronary blood supply

-Myocardial infarction (narcosis) =MI
Prolonged ischemia causing irreversible damage and cell death

s/s:

22
Q

Hematology:

Hemostasis

A

1) Vascular spasm/Vasoconstriction (reducing blood flow)

2) Platelet Plug Formation (wad of gum in the hole):
-Platelet activation (Calcium required); immobilizing meshwork of platelets and fibrin
-Adhesion of platelets to damaged vascular wall by
von Willebrand factor (vWF)

3) Coagulation/Formation of Fibrin Clot (gum won’t hole forever, so we cement of the gum and hole)
4) Clot retraction: actin-like contractile proteins in the platelets
5) Fibrinolysis

23
Q

Hematology: Anemias
Macrocytic Normochromic- generally, what is the result for RBC?

1) Pernicious
2) Folate Deficiency

A

Decreased lifespan of RBC
1) Pernicious: Lack of intrinsic factor from gastric parietal cells leading to decreased B12 absorption.

2) Folate Deficiency: Not dependent on another factor; decreased folate absorption in the sm. intestine.

24
Q

Hematology: Anemias
Microcytic Hypochromic- generally, what is the result for RBC?

3) Iron Deficient
4) Sideroblastic
5) Thalassemia

A

Small in size; decreased number of Hgb
3) Iron Deficient: Nutritional; metabolic/ functional.

4) Sideroblastic: Altered mitochondrial metabolism leading to insufficient iron uptake and dysfunctional Hgb synthesis.
5) Thalassemia: Genetic; production of malformed Hgb chains.

25
Q

Hematology: Anemias
Normocytic Normochromic- generally, what is the result for RBC?

6) Aplastic
7) Post hemorrhagic
8) Hemolytic
9) Sickle cell
10) Chronic Inflammation

A

Not enough RBC in circulation.
6) Aplastic: A: pancytopenia- ALL blood cells are deficient= bone marrow issue.
B: Pure RBC aplasia- RBC are not being made leading to decreased EPO= issue in the kidney.

7) Post hemorrhagic: acute blood loss from trauma.
8) Hemolytic: spleen enlargement= accelerated RBC destruction (may cause Jaundice); Lupus.
9) Sickle cell: Genetic; RBC “sickle”; risk of CVA.
10) Chronic Inflammation: AIDS; RA; Lupus: hepatitis; renal failure; malignancies.

26
Q 
Digestive:
Gastroesophageal reflux (GERD)
A

Reflux of chyme from stomach to esophagus

If GER causes inflammation of the esophagus, it is called reflux esophagitis

Normal functioning lower esophageal sphincter maintains high pressure to prevent chyme reflux

Conditions that increase abdominal pressure or delay gastric emptying can contribute to GERD

27
Q

Digestive: Peptic Ulcers

Duodenal ulcers

A

Most common of the peptic ulcers

Helicobacter pylori infection (H. pylori)
Toxins and enzymes that promote inflammation and ulceration
primarily comes from ingestion of fecal matter

Use of NSAIDs
Hypersecretion of stomach acid and pepsin
Acid production by cigarette smoking

Hematemesis (coffee grounds), melena

28
Q

Digestive: Peptic Ulcers

Gastric ulcers

A

Tend to develop in the antral region (pylorus) of the stomach

Most common causes are use/overuse of NSAIDs, H. pylori, gastritis, alcohol

Hematochezia

29
Q

Digestive: Peptic Ulcers

Esophageal ulcers

A

Most commonly caused by GERD

Others include: use of NSAID’s, smoking, effects of forced vomiting in Bulimia cases

Hematemesis (coffee grounds)

30
Q

Digestive:
Hepatic Portal HTN
Cause
Effect

A

Abnormally high blood pressure in the portal venous system caused by resistance to blood flow.

1) Intrahepatic: causes occur from vascular remodeling with thrombosis, inflammation, or fibrosis of the capillaries; result of cirrhosis or viral hepatitis.
2) Posthepatic: causes occur from hepatic vein thrombosis or right ventricle cardiac disorders; causes blood to collect.

-Splenomegaly: spleen becomes enlarged.
-Ascites: decreased synthesis of albumin by the liver.
-Hepatic (liver) encephalopathy (disease of the brain):
accumulated toxins alter and interfere with neurotransmission, and cause edema. Most commonly ammonia, which cannot be converted to urea by the diseased liver

31
Q

Urinary:

The 3 steps of urine formation

A

1) Filtration (filtration slits): of blood into tubules. Nonselective: driven by hydrostatic BP= we lose things we want (glucose, water, Na+). A small amount of ammonia is also able to pass.
2) Reabsorption: from tubules back into the blood. Selective: Mostly occurs in the PCT (water, Na+, ALL the glucose); Loop of Henle causes concentration (water, Na+).
3) Secretion: from blood into tubules. Selective, what we want to trash: Mostly occurs in the DT and CD (ammonia, urea, H+, K+). Also pH regulation …HCO3- and H+.

32
Q

Urinary: UTIs

1) Acute cystitis

A 
1) Cystitis is an inflammation of the bladder; Most common pathogen is Escherichia coli.
s/s: Frequency, dysuria, urgency, and lower abdominal and/or suprapubic pain, pain with urination
Cloudy urine (main symptom, due to inflammatory exudate), fever, hematuria (blood in urine).
33
Q

Urinary: UTIs

2) Acute pyelonephritis
3) Chronic pyelonephritis

A

2) Acute infection of renal pelvis and/or kidney interstitium (fluid space).
Common causes: E. coli, renal calculi, ureteral reflux, pregnancy, neurogenic bladder (CNS damage), catheterization.

3) Persistent or recurring episodes of acute pyelonephritis that leads to scarring: impairs kidney function.
Risk of chronic pyelonephritis increases in individuals with renal infections and some type of obstructive pathologic condition.

34
Q

Urinary:
Glomerulonephritis
Cause
Effect

A

Effects filtration leading to GFR impairment.
-Primary glomerular injury: Isolated inflammatory response in kidney (type III hypersensitivity- post strep infection).

-Secondary glomerular injury: Caused by some other systemic disease (Eg: type II hypersensitivity- Lupus, DM, HTN)

Increased glomerular capillary permeability (hypoalbuminemia); decreased GFR; increase BUN

35
Q 
Urinary: 
Acute Kidney Injury (AKI)
Cause 
Effects
s/s
A
  • Most commonly caused by sudden impaired renal blood flow. Eg: major blood loss from trauma or hypovolemic shock that decreases MAP.
  • GFR declines because of the decrease in filtration pressure.
  • Oliguria (production of abnormally small amounts of urine) and anuria (no urine production)
36
Q 
Urinary: 
Chronic Renal Failure (CKD)
Cause 
Effects
s/s
A
  • Irreversible loss of renal function that affects nearly all organ systems, over a period of time.
  • Causes: HTN, diabetes, lupus, other autoimmune.
  • Proteinuria and uremia (increased BUN)
  • Creatinine and urea clearance (decreased)
  • Fluid, electrolyte and acid-base imbalance
  • Anemia (aplastic: aplasia)
  • Hypocalcemia (b/c of low vit. D released by the kidney)

Dialysis, supplement EPO, Vit. D, transplant list.

37
Q

Musculoskeletal:
Osteomyelitis
Cause
Effect

A

A bone infection most often caused by staph. infection

  • Common cause is open wound (exogenous) spread; or from a blood-borne (endogenous) infection.
  • Inflammation forms exudate that lifts the periosteum and disrupts blood vessels which deprives underlying bone of its blood supply leading to narcosis.
  • Acute and chronic inflammation, fever, pain, necrotic bone
38
Q

Musculoskeletal:
Osteoporosis
Cause
Effect

A

Reduced bone mass/density and an imbalance of bone resorption and formation (Too much osteoclasts not enough blasts).

  • Decreased levels of estrogen (menopause) and testosterone; Decreased activity level (age related).
  • Fragile bones
  • excessive PTH, low vit D
39
Q

Musculoskeletal: Inflammatory joint disorders

RA

A

Systemic autoimmune damage to connective tissue, primarily in the joints (synovial membrane)

Characterized by inflammatory damage or destruction in the synovial membrane or articular cartilage and by systemic signs of inflammation
Fever, leukocytosis, malaise, anorexia, and generalized aching and stiffness

40
Q

Musculoskeletal: Non-inflammatory joint disorders

OA

A

Degeneration and loss of articular cartilage, sclerosis of bone underneath cartilage, and formation of bone spurs (osteophytes)

Also referred to as degenerative joint disease

Suspected Causes
Incidence increases with age, joint trauma, long-term mechanical stress

Pain, stiffness, enlargement of the joint, tenderness, limited motion, and deformity

41
Q

Musculoskeletal: Inflammatory joint disorders
Gout
Cause
s/s

A

Metabolic disorder that disrupts the body’s control of uric acid production (deposited in soft connective tissue) or excretion (kidney problem).
-Occurs when the uric acid concentration increases to high enough levels to crystallize and deposit in connective tissues throughout the body.

-s/s: high levels of uric acid in the blood and other body fluids
When these crystals occur in the synovial fluid, the inflammation is known as “gouty arthritis”

42
Q

Musculoskeletal: Inflammatory joint disorders
Ankylosing Spondylitis
Cause
s/s

A

Inflammatory systemic autoimmune joint disease of the spine or sacroiliac joints causing stiffening and fusion of the joints.

  • Begins with the inflammation of fibrocartilage, particularly in the vertebrae and sacroiliac joint
  • As repair begins, the scar tissue ossifies and calcifies; the joint eventually fuses
  • s/s: Low back pain, stiffness, pain, and restricted motion
43
Q

Integumentary:

Pressure Ulcers- staging

A

SI - Nonblanchable erythema of intact skin; Narcosis of hypodermis.

SII - Partial-thickness skin loss involving narcosis epidermis or dermis.

SIII - Full-thickness skin loss involving damage or loss of epidermis down to subcutaneous tissue.

SIV - Full-thickness skin loss with damage to muscle, bone, or supporting structures.

44
Q

Integumentary:

Fungal Infections

A

Fungi causing superficial skin lesions are called dermatophytes

Fungal disorders are called mycoses; mycoses caused by dermatophytes are termed tinea
Tinea capitis (scalp)
Tinea pedis (athlete’s foot)
Tinea corporis (ringworm)
Tinea cruris (groin, jock itch)
Tinea unguium (nails) or onychomycosis
45
Q

Integumentary:

Fungal Infections- Candidiasis

A

Caused by Candida albicans (yeast).
Normally found on the skin, in the GI tract, and in the vagina.
C. albicans can change from a commensal organism to a pathogen

46
Q

Integumentary:

Burn staging

A

1) First degree: Partial-thickness burns= involves epidermis only.
2) Second degree: Superficial and deep partial= involves epidermis and some/ all of the dermis (blister).
3) Third degree: Full-thickness burns= involves epidermis, dermis, and some/ all of the hypodermis.

47
Q

Systolic heart failure

A

Inability to generate adequate cardiac output to perfuse tissues (HTN, MI)
Ventricular remodeling or loss of myocytes

48
Q

Diastolic heart failure

A

Pulmonary congestion despite normal stroke volume and cardiac output (prolonged HTN). fluid into lungs
Ventricles can’t fill with blood because they won’t relax or are too thick

Patho: pulmonary; cardi; hemo; GI; Urinary (10 decks)

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