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Patho Exam 1 Review Study Guide
Information taken from provided Exam 1 review. Notes added form Wunderlich’s and Varges’ SoundCloud reviews online. *things Varges stressed in blue. Week 1 & 2: Cellular Biology A. Main components of the cell a. Nucleus i. What does it contain? (1)
- The nucleolus a. What is the nucleolus composed of (4): i. RNA ii. Most of the cellular DNA iii. The DNA-binding proteins iv. The histones 1. What do histones do? (1) a. Regulate activity 2. Why are histones important? (2) a. DNA chain in eukaryotic cells are so extensive the risk of breakage is high b. Histones bind to DNA and fold it into chromosomes which is essential to cell division b. Ribosomes i. What are they (1)?
- RNA-protein complexes (nucleoproteins) that are synthesized in the nucleolus ii. How do they get to the cytoplasm?
- Through pores in the nuclear envelope called nuclear pore complexes (NPCs) iii. Where can they be found (2)?
- May float free in the cytoplasm
- Attached to the outer membrane of the endoplasmic reticulum (ER) iv. What is their chief function?
- Provide sites for cellular protein synthesis c. Golgi Complex i. What is it also known as?
- Golgi apparatus ii. How would it be described?
- A network of flattened, smooth membranes and vesicles frequently located near the nucleus of the cell iii. What does it do?
- Takes proteins from the ER are processes/packages them into small membrane-bound sacs/vesicles called “secretory vesicles”
- Refines them and directs traffic in the cell a. What are three examples of what is refined and packaged? i. Proteins, polynucleotides, and polysaccharides d. Lysosomes i. How do they maintain cellular health (4)?
- Efficient removal of toxic cellular components
- Removal of useless organelles
- Termination of signal transduction
- Signals cellular adaption
ii. How does aging affect lysosomes?
- Leads to progressive loss of lysosomal efficiency which declines the regenerative capacity of organs and tissues iii. What functions do lysosomal components integrate?
- Nutrient abundance
- Energy levels
- Cell stressors a. What do lysosomes do with this information? i. Translate them into instructions that regulate cellular metabolism toward either proliferation or inactivity e. Mitochondria i. What are they responsible for?
- Cellular respiration and energy production ii. What does the inner membrane contain?
- Enzymes of the respiratory chain – the name given to electron-transport chain a. What are these essential to? i. The process of oxidative phosphorylation that generates most of the cell’s ATP iii. The mitochondrial matrix contains what kinds of pathways (1), involve what 2 things, and metabolize what 3 things (2)?
- Metabolic
- Urea and heme synthesis
- Carbs, proteins, and amino acids B. Apoptosis vs. Necrosis a. What can accumulate intracellularly caused by stresses from metabolic derangements (3)? i. Carbs, proteins, and lipids b. What are those important changes? Why? i. Nuclear – without a healthy nucleus the cell can’t survive c. What are the two main types of cell death? i. Necrosis and apoptosis d. Define apoptosis. i. Programmed cell death that’s regulated or programmed ii. Cellular self-destruction for elimination of unwanted cell populations e. Necrosis i. What characterizes it (3)?
- Rapid loss of the plasma membrane structure
- Organelle swelling
- Mitochondria dysfunction ii. What is the #1 cause of cellular injury leading to necrosis? Especially in what two organs?
- Hypoxia
- Heart and kidneys
E. Free Radicals a. Sodium and water can enter the cell freely, and cellular swelling results (decreases ability to properly function) a. Where do they plan a major role? i. Initiation and progression of diseases b. What is a free radical? i. An electrically uncharged atom or group of atoms having an unpaired electron c. What is wrong with an unpaired electron? i. Makes the molecule unstable (causes chemical imbalance of cell membrane) d. How do they try to stabilize? i. Gives up an electron to another molecule or by stealing one e. Why is this bad? i. Injurious chemical bonds can form with proteins, lipids, and carbs (they
destroy the cellular membrane) fight this by producing antioxidants
through healthy nutritious intake (neutralize)
f. What five diseases are said to affected by reactive oxygen species? When? i. In the initiation and progression of cardiovascular alterations associated with HL, DM, HTN, IHD, and CHF F. Cellular Injury a. What is a consequence of leakage of lysosomes during chemical injury? i. Enzymatic digestion of cellular organelles, including the nucleus and nucleolus, ensues, halting synthesis of DNA and ribonucleic acid (RNA) b. What happens when liver enzymes metabolize ethanol into acetaldehyde? i. Hepatic cellular dysfunction c. What happens when peroxisomes dysfunction, considering the liver?
i. Ethanol is turned into fat and thus fatty liver occurs (also causes dysfunction in
kupfurr cells)
d. What is ionizing radiation (IR)? What does it result in? i. Any form of radiation capable of removing orbital electrons from atoms ii. The production of negatively charged free electrons and positively charged ionized atoms e. What is ionizing radiation emitted from? i. X-rays, y-rays, and alpha and beta particles (which are emitted from atomic
nuclei in the process of radioactive decay) PUT ON A LEAD APRON
ii. Subatomic particles such as neutrons, deuterons, protons, and pions
f. What is a main mechanism of damage to DNA by ionizing radiation?
i. From generation of reactive oxygen species from reactions with free
radicals by radiolysis of water IT HURTS THE DNA THE MOST
G. Aging and the Cell/Tissues a. What happens with physiologic processes with age? i. Show to function less efficiently b. What is sarcopenia?
i. Muscular atrophy: degenerative skeletal muscle loss; how fast it
happens depends on nature/nurture
c. What happens when “stiffness” or “rigidity” of systems occurs?
i. Peripheral vascular resistance increases (i.e. HTN)
ii. Decreased production of HCL and delayed emptying of stomach (see a decrease
in appetite)
iii. Decreased immune response to T-dependent antigens d. What happens with fluid and electrolytes with aging? Why?
i. Total body potassium concentration decreases because of decreased cellular mass
vii. Leaning disabilities
viii. Neuromas J. Cystic Fibrosis a. CF is caused by what type of gene? i. Autosomal recessive b. Who does CF affect most? i. The most lethal autosomal recessive disease in white children c. How does someone get CF? i. The individual must be homozygous for a recessive allele to express the disease d. What about the carriers of CF? Why? i. Usually carriers are phenotypically normal ii. Most recessive alleles are maintained in normal carriers; they are able to survive in the population from one generation to the next K. Breast cancer a. What form of gene accounts for approximately 5% of breast cancer in the US? i. Autosomal dominant form b. Which genes are responsible for this form of breast cancer? i. Chromosome 17 (BRCA1) and 13 (BRCA2) c. What is the chance of a lifetime risk of developing breast cancer for women who inherit the BRCA1 or BRCA2? i. 50-80% d. Is it strong familial? i. Yes e. What is the risk of developing breast cancer if a woman has one affected first-degree relative? i. Doubled risk L. Diseases in populations a. How common is a given disease in a population? i. Well-established measures are used to answer this question b. What is the definition of incidence rate? i. The number of new cases of a disease reported during a specific period (typically 1 year) divided by the number of individuals in the population c. What is the definition of relative risk? i. A common measure of the effect of a specific risk factor d. How is relative risk expressed? i. A ratio of the incidence rate of the disease among individuals exposed to a risk factor divided by the incidence of the disease among individuals not exposed to a risk factor
EXAMPLE: The incidence of death from lung cancer was 1 .66 (per 1000 person-years) in heavy
smokers (more than 25 cigarettes daily), but it was only 0.07 in the nonsmokers. The ratio of
these two incidence
Week 3: Fluid (all dependent on ECFV/ICFV) P. Dehydration a. Name EIGHT signs and symptoms of dehydration: i. Headache ii. Thirst iii. Dry skin iv. Dry mucous membranes
(gums)
v. Elevated temperature
vi. Weight loss (except w/
edema)
vii. Decreased/concentrated urine viii. Skin turgor normal or decreased
(nor great) so look at tongue
b. Name FOUR signs and symptoms of hypovolemia:
i. Tachycardia (compensatory)
ii. Weak pulses iii. Dizziness
iv. Postural hypotension (r/t inability to compensate needed for equilibrium)
c. What receptors cause us to feel thirst? How are they activated? i. Osmoreceptors are activated by an increase in osmotic pressure of the plasma d. Name three populations vulnerable to fluid volume deficit (FVD):
i. Infants: 75-80% total body water (TBW) ( distribution of ECF more available)
ii. Obese: fat is water repelling ( BMI >30)
iii. Elderly: thirst sensation is diminished Q. Fluid Movement a. What is interstitial space? i. Tissue space b. What is oncotic pressure? i. Aka Colloid osmotic pressure – it is pressure exerted by proteins, notably albumin, in the blood vessel’s plasma that tends to pull water into the circulatory system c. Explain how fluid moves from the intravascular space into the interstitial space. What is in influenced by? i. Through the arterial end of capillaries and capillary hydrostatic pressure
(think about the heart – geṄng fluid/nutrients where they need to go) being
higher than the capillary oncotic pressure ii. Cardiac system d. What is oncotic pressure heavily influenced by? i. Plasma pressure e. What does ↓ plasma protein (albumin) cause? Why? i. Edema because of a reduction in plasma oncotic pressure R. Natriuretic peptides a. What are natriuretic peptides? i. Hormones b. Name THREE of the natriuretic peptides. What are they produced by/associated with? i. Atrial natriuretic peptide (ANP) produced by the myocardia atria ii. Brain Natriuretic peptide (BNP) produced by the myocardia ventricles iii. Urodilatin within the kidney c. What two things do natriuretic peptides affect? i. ↓BP and ↑ of sodium and water excretion d. What is are natriuretic peptides antagonists of?
i. The RAAS system (NPs are weak antagonist, though)
e. What does RAAS stand for? i. Renin angiotensin-aldosterone system f. What is renin? i. An enzyme secreted by the juxtaglomerular cells of the kidney g. Explain RAAS. i. Circulating blood volume/pressure is reduced felt by the kidneys ii. Renin, is released
- In response to what two things? a. Sympathetic nerve stimulation and decreased perfusion of the renal vasculature iii. Angiotensin I Angiotensin II iv. Aldosterone pumped out by adrenals (this is the main hormone released to increase perfusion)
- How does it do this? a. Controls ↑ sodium and therefore ↑storage of BP/water h. What is ADH? i. The antidiuretic hormone i. What causes secretion of ADH and the feeling of thirst? i. An increase in plasma osmolality (works with sodium) ii. (released by Posterior pituitary) conserves the water
j. Think hypovolemia aker stabbing incident (RAAS and ADH work together)
ii. Massive trauma iii. Insulin deficiency iv. Addison’s disease
v. Use of potassium salt subs (or K+ rich food) vi. Metabolic acidosis e. What happens when the ECF K+ increases without significant change in ICF K+? i. The resting membrane potential becomes more positive(look at the illustration to understand)
- What does that cause? a. The cell membrane becomes HYPOpolarized (inside becomes less negative) i. How would we see this on the EKG? 1. Tall peaked T waves f. Why do we often see hyperkalemia and acidosis together? i. Hydrogen ions shift into the cells in exchange for ICF potassium g. How is insulin used to treat hyperkalemia? i. Insulin transports K+ from the blood to the cell along with glucose h. How does insulin contribute to the regulation of plasma potassium levels? i. By stimulating the Na+, K+ ATPase pump which moves K+ into liver/muscle cells and glucose transport after eating i. What are the causes of hypokalemia? i. Hyperaldosteronism causes hypokalemia, hypernatremia, and fluid volume excess j. What are the signs and symptoms of hypokalemia? i. CARDIAC - Flattened T-waves, AV block, bradycardia ii. paralytic ileus (nausea/vomiting) U. Calcium (8.5-10.5 mg/dl) a. What causes hypocalcemia (8)? i. Inadequate GI absorption
ii. Massive blood
administration
iii. Deceases in PTH and
vitamin D levels
iv. Nutritional
deficiencies – malnutrition
v. Alkalosis
vi. Elevated calcitonin level
vii. Pancreatitis (soapy
stuff sequesters
calcium)
viii. Hypoalbuminemia
(calcium can’t hold
onto it)
b. Signs of hypocalcemia (5)?
i. Increased
neuromuscular excitability
ii. Tinging
iii. GI cramping
iv. Hyperactive bowel sounds
v. Osteoporosis/fractures
c. SEVERE signs of hypocalcemia (3)?
i. convulsions/tetany, prolonged QT interval (prolonged refractory period), cardiac
arrest
d. What is hypercalcemia caused by (6)?
i. Hyperparathyroidism
ii. Bone metastases with calcium released from breast, prostate, renal, and cervical
cancer
iii. Sarcoidosis
iv. Excess vitamin D
iv. Dysrhythmias, bradycardia, cardiac arrest
v. Bone pain, osteoporosis, fractures
f. Calcium and phosphorus have what kind of relationship? Influenced by what
three things?
i. Reciprocal; PTH, calcitonin, vitamin D
V. Phosphate (2-4.7 MG/DL) (think
respiratory)
a. What causes hypophosphatemia (5)? i. GI malabsorption r/t VIT D deficiency ii. Use of mag/aluminum antacids iii. Long term alcohol abuse iv. Respiratory alkalosis v. Increased renal excretion of phosphate associated with hyperparathyroidism b. What are the symptoms of hypophosphatemia related to? Name them. i. Conditions related to reduced capacity for O2 transport by RBCs and disturbed energy metabolism
- Leukocyte/platelet dysfunction
- Deranged nerve/muscle function c. Name 8 SEVERE symptoms of hypophosphatemia. i. Irritability/confusion ii. Numbness/coma/convulsions iii. Respiratory failure r/t muscle weakness iv. Cardiomyopathy v. Bone resorption (leading to rickets or osteomalacia) d. What are FOUR causes of hyperphosphatemia? i. Acute or chronic renal failure with loss of GF ii. Treatment of metastatic tumors with chemotherapy that releases large amounts of phosphate into serum iii. Long term use of laxatives/enemas containing phosphates iv. Hypoparathyroidism e. What are the symptoms of hyperphosphatemia? i. Symptoms primarily related to low serum calcium levels (caused by high phosphate levels) ii. If prolonged – calcification can occur to soft tissues W. Magnesium (1.5 – 3 mEq/L) a. What are FOUR causes of hypomagnesemia? i. Malnutrition ii. Malabsorption syndromes iii. Alcoholism iv. Urinary losses (rental tubular dysfunction, loop diuretics) b. What are NINE symptoms of hypomagnesemia? i. Behavioral changes (irritability) ii. Increased reflexes, muscle cramps iii. Ataxia, nystagmus, tetany, convulsions iv. Tachycardia, hypotension c. What are FOUR causes of hypermagnesemia? i. Renal insufficiency or failure (most common) ii. Excessive intake of magnesium-containing antacids iii. Adrenal insufficiency
d. What are NINE symptoms of hypermagnesemia?
Z. Metabolic Acidosis
a. What causes this? Two types 1. Taking in acid 2. Loss of bicarb
i. Increased non-carbonic acids (elevated anion gap)
- K - Ketones (DKA)
- I - ingestion
- L – lactic acid
- U – uremia/uremic acid ii. Bicarbonate loss (normal anion gap)
- Diarrhea
- Ureterosigmoidostomy
- Renal failure
- Proximal renal tubule acidosis b. What is the pathophysiology? i. Gain of fixed acid ii. Inability to excrete acid or loss of base c. What is the compensatory response? i. Increased CO2 excretion by lungs (Kussmaul respirations) d. Laboratory findings? i. Acidic pH ii. Normal CO2 (uncompensated) iii. Basic CO2 (compensated) iv. Acidic HCO AA. Metabolic Alkalosis a. What causes this? i. Vomiting ii. Nasogastric suctioning iii. Diuretic therapy
iv. Hypokalemia (potassium goes into cell and hydrogen ion will come out)
v. Excess NaHCO3 intake vi. Mineral-corticoid use b. What is the pathophysiology? i. Loss of strong acid or gain of base c. What is the compensatory response? i. Increased CO2 retention by lungs d. Laboratory findings? i. Basic pH ii. Normal CO2 (uncompensated) iii. Acidic CO2 (compensated) iv. Basic HCO
