Patho midterm study guide Flashcards

1
Q

Cellular catabolism

A

The process by which cells break down larger, complex molecules (like glucose, fats, proteins) into smaller, simpler ones, releasing energy in the form of ATP (adenosine triphosphate)

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2
Q

Steps to cellular catabolism

A

If oxygen present:
1. Glycolysis: breakdown glucose
2. Pyruvate decarboxylation: Forms acetyl-CoA- releasing carbon dioxide and NADH
3. Citric Acid Cycle (Krebs cycle): Acetyl-Cot enters citric acid cycle broken down, and and releases carbon dioxide and transferring electrons to NADH and FADH2
4. Oxidative Phosphorylation: chemiosmosis. Produces the majority of ATP

If no oxygen:
Fermentation: If oxygen is not present (anaerobic conditions) cells may resort to fermentation. Pyrate converted to lactic acid. Does not produce much ATP.

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3
Q

ATP

A

adenosine triphosphate. Serves as the primary energy carrier in all living cells.

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4
Q

5 types of cellular/tissue changes in response to stimuli/conditions

A
  1. Hypertrophy: increase in cell size
  2. Atrophy: decrease in cell size
  3. Hyperplasia : increase in NUMBER of cells
  4. Metaplasia: change from one cell type to another
  5. Dysplasia: abnormal growth of cells that may lead to cancer
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5
Q

Hypertrophy
Cause and example

A

Increase in cell/tissue SIZE

occurs in response to increased workload/hormones

Example: weight training/exercise.
Example 2: hypertrophy of cardiac cells due to increased blood pressure/workload

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6
Q

Atrophy
Cause and example

A

decrease in cell/tissue SIZE

occurs due to decreased workload, lack of nutrition, gaining, decreased blood supply

Example: Best rest: Muscle cells atrophy

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7
Q

Hyperplasia
Cause and example

A

Increase in the NUMBER OF CELLS

cause: increase hormonal stimulation, chronic irritation, or healing mechanisms

Example: Endometrial hyperplasia: increased number of cells lining the uterus due to hormonal imbalances.

Example 2: Enlarged prostate due to Benign prostatic HYPERPLASIA

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8
Q

Metaplasia
cause and example

A

Is the REVERSIBLE CHANGE of one differentiated cell type to another

cause: adaptive response to stress or injury

example: respiratory tract ciliated epithelial cells transform to squamous epithelial cells in response to chronic smoking

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9
Q

Dysplasia

A

Abnormal development or growth of cells
*Precursor to cancer

Cause: chronic inflammation, irritation, exposure to carcinogens

Example: Cervical dysplasia (usually caused by HPV)

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10
Q

What is nuclear division in cell reproduction called?

A

Meiosis: Occurs only in germ (sex) cells

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11
Q
A
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12
Q

Function of RNA

A

Create proteins via translation

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13
Q

Four types of tissue (form organs with specific functions)

A
  1. Epithelial tissue: line outside and interior areas of body (skin, lining of GI tract, respiratory tract, blood vessels)
  2. Connective Tissue: Provides support. Adipose, cartilage, bone, lymph
  3. Muscle tissue: Responsible for movement. ex. skeletal muscle (voluntary) and smooth muscle (involuntary ex. heart)
  4. Neural Tissue: Process/transmit info. Ex. brain spinal cord nerves
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14
Q

Epithelial tissue

A

Epithelial tissue: line outside and interior areas of body (skin, lining of GI tract, respiratory tract, blood vessels)

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15
Q

Connective Tissue:

A

Connective Tissue: Provides supports/bind other tissues together. adipose, cartilage, bone, blood lymph.

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16
Q

Muscle Tissue

A

Muscle Tissue: Responsible for movement. Voluntary and involuntary movement. Ex. Skeletal muscle (voluntary movement) and smooth muscle (involuntary movement ex. Heart)

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17
Q

Neural Tissue

A

Neural Tissue: Neural cells/neurons. Process/transmit info. Ex. Brain, spinal cord, nerves

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18
Q

Molecular transport that requires energy

A

Active transport: The movement of a substance from an area of lower concentration to an area of higher concentration against a concentration gradient.

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19
Q

Describe active transport

A

Primary vs. secondary:
Primary: Uses energy directly obtained from ATP
-3 systems use it.
Sodium-potassium ATPase. (cardiovascular)
Calcium-pump (muscular)
Potassium-hydrogen pump (proton pump) (GI function)

Secondary active transport:
uses energy stored from sodium-potassium pump (NOT ATP) and other molecules tag along with sodium to enter the cell.
-Neurotransmitters such as serotonin or norepinephrine move using secondary active transport

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20
Q

Function of the endoplasmic reticulum

A

smooth or rough. Function to produce proteins for the rest of the cell to function.

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21
Q

11 parts of cellular function

A
  1. Metabolism (catabolism vs. anabolism)
  2. Protein synthesis
  3. Cell division (mitosis vs. meiosis)
  4. Energy production (cellular respiration vs. fermentation)
  5. Transport of molecules (active vs. passive transport)
  6. Cell signaling
  7. Homeostasis
    8.Waste removal
  8. Structural support:
  9. Cellular communication/interaction
  10. Apoptosis (programmed cell death)
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22
Q

Function of the lipid bilayer cell membrane

A

Membrane that separates the cell from the external environment. Made up of two layers of phospholipids. Cell membrane surrounds the cell.

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23
Q

What is an electrolyte

A

A substance that, when dissolved in water, dissociates into ions (charged particles)
Types of electrolytes:
Cations: (positive charged ions) example sodium, potassium, calcium, mg

Anions: Negatively charged ions
example chloride, bicarb, phosphate

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24
Q

Function of electrolytes

A
  1. fluid balance in and out of cells
  2. nerve function/transmission to generate electrical impulses
  3. muscle function: muscle contraction and relaxation
  4. acid base balance
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25
Q

Who is at risk for hypernatremia?

A

People who do not drink enough water or lose too much water.
Ex: Elderly, infants, alzheimrs, sweating (dehydration), D/V, kidney disease

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26
Q

What electrolyte has the highest concentration in the ICF?

A

ICF= POTASSIUM

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27
Q

What electrolyte has the highest concentration in the ECF?

A

ECF= Sodium

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28
Q

What determines osmotic pressure?

A

the concentration of solutes in a solution.

Osmosis is the movement of water from an area of low solute concentration to an area of high solute concentration to balance both sides of the membrane.

Osmotic pressure is mainly determined by the solute concentration, the number of particles, the solute dissociates into, and the temperature of the solution.

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29
Q

How does water move through the lipid bilayer cell membrane?

A

Osmosis allows water to slowly diffuse through the lipid bilayer. Aquaporins are specialized channels that facilitate much faster water transport across the membrane.
Both processes help the cell maintain osmotic balance and manage water intake and loss effectively.

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30
Q

What is the ratio of bicarbonate and carbonic acid to maintain pH at 7.4?

A

20:1.

this means that for every 1 molecule of carbonic acid
in the blood, there should be about
20 molecules of bicarbonate to keep the pH around 7.4,

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31
Q

What determines water movement between ECF and ICF?

A

Osmotic forces

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32
Q

What is most responsible for osmotic pressure?

A

Ions and glucose contribute to 95% of the osmotic pressure as they are the most abundant in the serum.
Osmolality and, subsequently, osmotic pressure are not affected by the size or charge of the solutes but only by the number of solutes.

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33
Q

What is the major buffering system in the ECF?

A

The Bicarbonate Buffer System. The major buffer system in the ECF is the CO2-bicarbonate buffer system. This is responsible for about 80% of extracellular buffering.

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34
Q

Who is most likely to have dehydration?

A

Infants and young children
older adults (elderly)
people with chronic illness
athletes
fever/illness
pregnant/breast feeding

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35
Q

Why are elderly more at risk for dehydration?

A

Why: As people age, the body’s ability to conserve water diminishes. Older adults often have a reduced sense of thirst and may not drink enough fluids. 
Also increase comorbidities and medication use.

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36
Q

Is the ICF and ECF isotonic?

A

Yes. They have the equal concentrations of solutes across a semipermeable membrane (and movement aka osmosis happens to keep it equal)

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37
Q

Male chromosomes

A

XY
-make them more likely to exhibit have X-linked traits because only 1 X and not another to help compensate

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38
Q

Female chromosomes

A

XX
Less likely to exhibit X-linked disorders because they have an additional normal X to compensate. Females need two copies of the mutated gene to exhibit defect however can be a carrier with one mutated gene.

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39
Q

Example of X-Linked recessive mutations

A

Hemophilia
Duchenne muscular dystrophy
Red-green colorblindness

^typically affect males

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40
Q

Down syndrome

A

Trisomy-21: A genetic condition caused by an extra copy of chromosome 21.
Most people have two copies of chromosome 21, down syndrome mutation has 3.

The extra genetic material affects development and causes characteristic physical and intellectual traits.

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41
Q

How many chromosomes do people have

A

46 chromosomes total (23 pairs for each parent)

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42
Q

Mosaic down syndrome

A

A rare form of Down syndrome where some sex cells in the body have two copies of chromosome 21 (normal) however others have 3 (abnormal)

Milder form of down syndrome depending on how many cells have mutation

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43
Q

Genotype vs. Phenotype

A

Genotype: The genetic material passed between generations (ex. BB, Bb, bb)

Phenotype: The set of observable physical traits from the genetic material. Ex purple verses white flower

44
Q

Autosomal recessive inheritance risk:

A

If you are born to parents who both carry the autosomal recessive gene (xX), you have a 25% chance of inheriting the variant gene and developing the disease (XX-because RECESSIVE).

You have a 50% chance of inheriting one variant gene and being a carrier (Xx)

45
Q

Oxygen-Hemoglobin dissociation curve

A

the relationship between the partial pressure of oxygen (pO₂) and the percentage of hemoglobin bound with oxygen (SaO2)

right shift: Give to tissues
left shift: Nothing LEFT for the tissues

46
Q

Complications of chronic bronchitis

A

Chronic bronchitis=type of COPD where chronic inflammation (smoking, chemicals) cause cytosine release which cause mucous production/chronic cough.
Can lead to:
1. Respiratory infections (the chronic mucous serves as breeding ground for virus/bacteria)
2. Pulmonary Hypertension: increased workload on the lungs can cause high blood pressure in the lungs and right sided heart failure (cor pulmonale-edema)
3. Respiratory failure: impairs the lungs ability to exchange oxygen and carbon dioxide. Lungs can no longer deliver sufficient oxygen to the bloodstream or remove enough carbon dioxide.
4. Lung cancer due to chronic irritation/cellular changes
5. chronic cough/mucus production
6. pulmonary embolism
7. oxygen dependence

Tx: quit smoking, bronchodilators, steroids, mucolytics!
vaccination

47
Q

Emphesema

A

Another type of COPD not caused by mucous production (unlike chronic bronchitis)

damage to the air sacs causing them to collapse during expiration- ineffectively get CO2 out

48
Q

Symptoms of pulmonary edema

A

Bloody sputum

49
Q

Virchow’s Triad

A

Factors that cause a DVT

  1. stasis of blood (immobility)
  2. Injury (damage to the blood vessel triggers clotting process)
  3. Hypercoagulatbility (due to genetic mutations ex. factor 5, cancer, pregnancy, oral contraceptives, dehydration due to thicker blood)
50
Q

Complications of Pulmonary embolism

A

PE occurs when Virchow’s triad comes together to form a DVT that travels to the lungs and obstructs pulmonary artery
1. acute respiratory failure
2. hypoxia
3. right sided HF
4. cariogenic shock: low BP, weak pulse, cold skin, confusion

*Less likely that the blood clot will travel to the brain to cause stroke because the clot would need to pass from right side of the heart to left side unless PFO

51
Q

Early stages of emphysema

A

Emphysema: Type of COPD (not caused by cytokine response) where aioli collapse due to decreased elastin (during expiration)

Early s/s: SOB with activity
-advanced lead to CO2 retention

52
Q

Most common characteristic with IPAH (idiopathic pulmonary artery HTN)

A

SOB on exertion
then leads to JVD/Right sided HF

(think brit)

53
Q

Causes of obstructive atelectasis

A

collapsed lung due to obstruciton
1. most common is surgery with anesthesia
2. foreign body aspiration (ex food)
3. mucus plugging (COPD, cystic fibrosis)
4. tumors
5. lung abcesses

54
Q

Chronic Obstructive Pulmonary Disease (COPD)

A

is a group of progressive lung diseases that cause airflow obstruction and breathing difficulties.

  1. Chronic bronchitis: long term inflammation leading to mucus production
  2. Emphysema: air sacs (alveoli) in the lungs get damaged and decreased surface area for gas exchange + decreased elastitisity of lungs. SOB + barrel chest
55
Q

Pathophysiology of chronic bronchitis

A

Chronic inflammation leads to Mucous metaplasia, a process in which mucus is overproduced in response to inflammatory signals, is the pathologic foundation for CB. The primary mechanisms responsible for excessive mucus in COPD are overproduction and hypersecretion by goblet cells and decreased elimination of mucus.

56
Q

Ventilation problems (three types)

A

Obstructive, restrictive, central

Ventilation problems refer to any issue that interferes with the movement of air into/out of the lungs

  1. obstructive problems: refers to the airways restrict flow of air into/out of the lungs (particularly during exhalation) ex. COPD/Emphesema
  2. Restrictive problems: lung/chest wall are unable to fully expand, limiting the total volume of air in. Ex. pulmonary fibrosis (stiff lung tissue), pleural effusion, obesity, pneumothorax,
  3. Central ventilation problems:
    issues with respiratory centers in the brain. Ex. central sleep apnea/guillian barre/ALS
57
Q

Pleural effusion fluid

A
  1. Transudative:
    Systemic factors that alter fluid imbalance causing fluid leaking from capillaries into the pleural space. Ex. CHF, Cirrhosis, (reduced albumin), low albumin

Characteristics of the Fluid: Clear, pale yellow fluid. Low protein content

  1. Exudative Pleural Effusion:
    Cause: local factors that increase the permeability of the pleural capillaries, allowing proteins, cells, and other substances to leak into the pleural space.
    Common Causes: Infections, Malignancy, Pulmonary embolism, Autoimmune diseases (rheumatoid arthritis, lupus), Pancreatitis. Post-surgical or post-traumatic
    Characteristics of the Fluid: Cloudy or turbid fluid (due to the presence of white blood cells and proteins).
  2. Chylous Pleural Effusion (Chylothorax)
    Cause: Chylous effusions are caused by the accumulation of lymphatic fluid, which is rich in triglycerides and occurs due to damage to the lymphatic vessels or obstruction of lymphatic flow. This may result from trauma, surgery, or malignancy. 

    Common Causes: Trauma, Malignancy, Congenital malformations, Infections
    Characteristics of the Fluid: Milky, white appearance (due to the presence of chylomicrons, which are rich in fat)
  3. Purulent Pleural Effusion (Empyema) -
    Cause: Purulent effusions, also known as empyema, occur due to infection that causes the pleural space to fill with pus. This typically results from a bacterial infection that spreads to the pleural space, most often after pneumonia or a lung abscess.
    
Characteristics of the Fluid: Cloudy, thick, yellow or greenish fluid. Very high white blood cell count, primarily neutrophils. Very high protein content.
58
Q

Pulmonary fibrosis and lung volume changes

A

Pulmonary fibrosis lung volume measurements are altered due to scarring of the lung tissue causing reduced ability to expand/contract.

Decreased values include: Total Lung Capacity (TLC), Vital Capacity (VC), and Forced Vital Capacity (FVC), due to the restrictive nature of the disease

RV (residual volume- air left in lungs after expiration) may be increased

FVC and FEV1 (forced expiratory volume in one second). FVC is reduced, but the ratio of FEV1/FVC is typically preserved (indicating restrictive disease)

59
Q

Patho + Cause of asthma

A

Patho:
1. Hyperresponsive airway causes inflammatory response T-helper cells and eosinophils.
2. Broncho restriction due to histamine lading to narrowing of the airways (wheezing/SOB)
3. mucus secretion due to goblet/leukotrienes (produced during inflammation)

causes: genetics, air pollution, tobacco smoke

60
Q

ARDS

A

Acute respiratory distress syndrome (ARDS) occurs when lung swelling causes fluid to build up in the tiny elastic air sacs in the lungs (alveoli). The fluid leaking into the air sacs keeps the lungs from filling with enough air. This means less oxygen reaches the bloodstream, so the body’s organs don’t get the oxygen they need to work properly.

ARDS usually occurs in people who are already critically ill or have major injuries. People usually are severely short of breath the main symptom of ARDS, within a few hours to a few days after the injury or infection that caused ARDS.

61
Q

Oliguria

A

Urine less than 400mL/day (or 20mL/hr)
*sign of advanced CKD

62
Q

Diet with CKD

A

Kidneys ability to filter waste/balance electrolytes decline with CKD:

  1. protein restriction to reduce buildup of urea/creatinine
  2. sodium restriction: Extra sodium can cause HTN and worsen CKD
  3. potassium control: In later stages of CKD can lead to hyperkalemia
63
Q

Which bacteria usually causes UTI (acute cystitis)?

64
Q

ESRD why at risk for bone fracture?

A

In final stages of CKD kidneys renal can cause renal osteodystrophy due to disruption in calcium and phosphate balance. In ESRD kidneys can no longer effectively excrete phosphate which leads to hyperphosphatemia. Extra phosphate can bind with calcium forming calcium-phosphate crystals which can lead to hypocalcemia. That leads to increased PTH hormone (secondary hyperparathyroidism) in response to low calcium levels. PTH acts to increase calcium levels by releasing calcium from the bones back into the blood and overtime leads to bone weakening.
Also, in ESRD kidneys are less able to convert Vitamin D to its active form.

65
Q

Bacteria that causes APSGN

A

Group A strep (GAS)

66
Q

Most common type of kidney stone

A

Calcium oxalate

67
Q

Patho of APSGN

A

GAS due to strep throat or Impetigo can lead to APSGN if it spreads to the kidneys. The immune system responds to the strep infection by producing antibodies against the bacteria. Then immune complexes circulate in the bloodstream and deposit in the glomeruli of the kidneys. The immune response causes inflammation in the glomeruli and impairs the kidneys ability to filter waste and lead to symptoms like: Hematuria, Proteinuria, edema, HTN.
Symptoms usually occur 1-3 weeks after the strep infection typically after the resolution of strep throat/impetigo. 
S/S: Dark colored urine, facial/peripheral edema, HTN, Decreased urine output, mild fever, fatigue
Dx: Based on clinical features such as hx of recent strep infeciotn, urinalysis shows hematuria/proteinuria, elevated creatinine,
Tx: most resolve without treatment. Supportive management to control BP, diuretics for edema, antibiotics if active strep infection.

68
Q

Causes of AKI pre-renal, intra-renal, post-renal

A

Pre-renal: Before the kidneys. Reduction of blood flow to the kidneys leading to decreased ability to filter waste. Usually due to issues with PERFUSION. Common causes: Hypovolemia, dehydration (vomiting, diarrhea, sweating), blood loss, burns, decreased cardiac output, heart failure, sepsis.
Intra-renal (intrinsic-within the kidneys): Direct damage to the kidney tissue. Common causes Acute tubular necrosis, Medications, Glomerulonephritis, post-strep glomerulonephritis, Bergers disease (IgA nephropathy)
Post-renal (after the kidneys): obstructive issues preventing urine from flowing freely out of the kidneys. Ex UTI, BPH, urethral stricture, kidney stones.

69
Q

Acute pylonephritis

A

Upper UTI infection

70
Q

Nephrotic syndrome

A

Damage to the glomeruli (filtering units of the kidneys). Biggest s/s is proteinuria (massive protein loss in urine). Also causes hypoalbuminemia, edema, hyperlipidemia.

71
Q

Cause of hydronephrosis and decreased GFR in kidney stones

A

Kidney stone cause hydronephorosis (swelling and dilation of the kidney) when they obstruct the urinary tract. The increased pressure from the backed up urine causes hydronephrosis and then decreased kidney function.

72
Q

RAAS system

73
Q

Juxtoglomerular complex

A

specialized structure in the kidney that plays a crucial role in regulating blood pressure and renal function through the Renin-Angiotensin-Aldosterone System (RAAS). 


74
Q

What are the functions of the kidneys

A
  1. Filtration of Blood: Removes waste products, toxins, and excess substances. 
2. Fluid Balance Regulation: Maintains appropriate hydration and urine concentration. 
3. Electrolyte Balance: Controls sodium, potassium, calcium, phosphate, and magnesium levels. 
4. Acid-Base Regulation: Maintains blood pH by excreting H+ and reabsorbing bicarbonate (HCO3-). 
5. Blood Pressure Regulation: Through the RAAS system and fluid regulation. 
6. Erythropoiesis: Stimulates red blood cell production via erythropoietin. 
7. Detoxification: Filters and eliminates metabolic waste and drugs. 
8. Vitamin D Activation: Converts vitamin D into its active form for calcium and phosphate regulation. 
9. Detoxification of Nitrogenous Wastes: Removes products like urea and creatinine. 
10. Osmolarity Regulation: Ensures the proper concentration of solutes in the body’s fluids. 

75
Q

WBC differential

A

granulocytes (neutrophils, eosinophils, basophils) and nongranulocytes (lymphocytes and monocytes)

WBC (leukocytes)= neutrophils, eosinophils, basophils, mastcells, lymphocytes

76
Q

Iron deficiency anemia:

A

Microcytic (low MCV) + hypochromic

77
Q

Macrocytic anemia

A

Macrocytic + Normochromic

*usually from b12 or folate deficiency

78
Q

Anemia of chronic disease

A

Normocytic + normochromic
RBC develop to maturity but chronic inflammation cause iron trapping. Likely due to cancer, CKD, CHF, infections

79
Q

Aplastic anemia

A

Normocytic + normochromic
Rare but serious.
Bone marrow fails to produce multi-potent it hemopoietic stem cells.

S/S: Pantocytopenia (low erythrocytes, low leukocytes, low thrombocytes)

Causes: Idiopathic conditions (lupas, RA), genetic abnormalities, cancer

80
Q

Causes of anemia due to inadequate production of RBC (4)

A
  1. Iron deficiency
  2. microcytic anemia
  3. anemia of chronic disease
  4. Aplastic anemia
81
Q

Causes of anemia excessive loss of RBC

A
  1. hemolytic anemia (sickle cell disease and thalassemia)
  2. Transfusion reaction
82
Q

Hemolytic anemia

A

Blood disorder that occurs when RBC are destroyed faster than they can be replaced
1. sickle cell diseae
2. Thalassemia

83
Q

Megaloblastic anemia

A

MCV > 100
caused by Vitamin B deficiency, folate defieicny, impaired DNA synthesis

Tx: Folic acid, B vitamins

*deficiencies can occur quickly

84
Q

Most common type of anemia

A

Iron deficiency anemia

cause: Inadequate iron supply

85
Q

If iron deficiency anemia caused by inadequate intake, reticulocytes will be:

A

Low (immature RBC)

86
Q

If iron deficiency anemia is caused by hemorrhage, reticulocyte will be:

A

High (immature RBC)

87
Q

Reticulocytes

A

Immature RBCs that circulate for 1-2 days until they mar into RBCs

88
Q

Hemolytic anemia s/s

A

Chills, abnormal paleness, jaundice, dark urine, fever, weakness, confusion, decreased physical activity

89
Q

Who gets B12 deficiencies?

A

Vegans/vegetarians- diet deficient. Animal meat, fish, eggs, dairy.

Most common cause: Pernicious anemia (antibodies attack gastric cells)

Autoimmune conditions: hashimotos, graves, DM 1)

90
Q

Pernicious anemia

A

Caused by autoantibodies (CD4-T cells) attack gastric cells

91
Q

Vitamin important in clotting

92
Q

Hemophilia A: What factor is deficient?

A

Genetic disorder. Factor 8 deficient (helps with clotting)
Tx: replace clotting factor 8 or 9

*Patients may be taught to give injection at home at first sign of bleeding

93
Q

Acute post streptococcal glomerulonephritis (APSGN)

A

Group A beta strep

*most common in young boys

Edema/HTN

Patho:antigen-antibody complex deposition in the glomerular capillaries cause inflammatory damage

94
Q

DIC what’s it stand for?

A

Disseminated intravascular coagulation

95
Q

What causes DIC?

A

Bacterial infection, sepsis, trauma from burns, blood transfusion reaction, pregnancy complications (retained placenta), severe liver disease, snake bites

96
Q

Symptoms of DIC?

A

Multi system organ damage (tachy, hypo). Bleeding problems (petechiae, epistaxis, hematuria)

clots clots clots, bleeds bleeds bleeds

97
Q

Lab values with DIC

A

CBC:
platelets decrease rapidly
PT/PTT: Prolonged clotting times
D-dimer: high
Low fibrinogen function

98
Q

Polycythemia vera: what is it and what causes it?

A

Above normal RBC/hemoglobin. Bone marrow produces too many RBC.

Two types: Primary vs secondary
Primary: Mutation in the Jak2 gene
Secondary: Due to disease such as COPD, pulmonary fibrosis, blood doping, androgens, steroids.

99
Q

Polycythemia vera: S/S

A

Visual disturbances, headache, splenomegaly pruritus with water, gouty arthritis

100
Q

Polycythemia vera lab levels:

A

CBC:
Increased Hemoglobin
low erythropoietin
JAK2 mutation

101
Q

Eosinophilia

A

Occurs with parasitic infection, malignancies, drugs.

Eosinophils help control inflammatory responses: asthma

102
Q

Sickle cell anemia causes

A

Gene abnormality. Mutation of the HBB gene
HgSS

103
Q

Sickle cell anemia S/S

A

Increased O2 demand (high-intensity exercise, high altitude), dehydration can precipitate sickling.

Crisis caused by obstruction of small vessels as sickle cells clog the vessels, leading to ischemia and necrosis. Triggered by dehydration, stress, high altitudes, fever, menses, and extreme temperatures. SEVERE PAIN

104
Q

Clot retraction and dissolution

A

After hemostasis, it follows another process called clot retraction, which stabilizes the clot by pulling together the wound edges of the vessel. Next, fibrinolysis occurs, which is an enzymatic process during which blood clots are dissolved to clear the way for blood circulation.

105
Q

Virchow’s Triad

A

Explains what causes DVTs
Venous stasis, hyper coagulability, and injuries to the endothelial cells that line the vessels.

Injury to the vein, due to bone fracture or surgery. Infection, slow blood flow from immobilization, genetics, family hx of VTE, high estrogen due to pregnancy, birth control, hormone replacement, blood clotting conditions such as factor V Leiden, polycythemia vera

106
Q

Stages of hemostasis

A

Stages of hemostasis:
(1) vascular spasm, or vasoconstriction, a brief and intense contraction of
blood vessels;
(2) formation of a platelet plug; and
(3) blood clotting or coagulation
Process by which bleeding is stopped: Primary and secondary
Decreasing blood loss: Endothelin and vasoconstriction, Platelet adhesion and von Willebrand
Factor (vWF). Release of serotonin, ADP, fibrinogen, calcium, thromboxane A2, Coagulation
cascade