Section 1

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4 states that will use apoptosis

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Last updated

6 years ago

Date created

Mar 1, 2020

Cards (69)

Section 1

(50 cards)

4 states that will use apoptosis

Front

1. severe cell injury 2. Accumulation of misfolded proteins 3. Infections (especially viral) Cytotoxic T cells induce apoptosis 4. Obstruction in tissue ducts In pancreas, kidney, parotid apoptosis, causes atrophy

Back

EKG hypokalemia

Front

slightly peaked P wave Slightly prolonged PR interval ST depression Shallow T wave Prominent U wave

Back

Atrophy

Front

Cell shape stays the same, decrease in size Physiologic- thymus gland as we develop shrinks Pathologic- Skeletal muscles from disuse, Aging causes brain cells and gonads to shrink

Back

CELL INJURY MECHANISM Result of Active cell injury

Front

immediate response of the entire cell

Back

Hyperkalemia EKG

Front

Peaked T wave wide flat P wave prolonged PR interval Decreased R amplitude widened QRS depressed ST segment

Back

Where does ROS occur

Front

Mitochondria most mitochondria lack catalase which makes the antioxidants inefficient

Back

CELL INJURY MECHANISM Result of Reversible injury

Front

Loss of ATP, cellular swelling, detachment of ribosomes, autophagy of lysosomes

Back

4 Mechanisms of Edema

Front

1. Increased capillary hydrostatic pressure 2. Decreased plasma oncotic pressure 3. Increased capillary membrane permeability 4. Lymphatic obstruction

Back

Hyperkalemia clinical manifestations

Front

Muscle weakness, atonality, paralysis, restlesness, cramps, diarrhea, low cardiac conductivity

Back

Cellular Adaption

Front

Cells adapt to protect themselves, at this point they are neither injured nor normal. somewhere in between

Back

Net filtration

Front

forces favoring filtration minus forces opposing filtration

Back

methods of Potassium intake and output Renal Regulation of potassium

Front

Intake- diet, meds or IV 50-100 mEq/day Output- urine and sweat Renal Regulation by: Aldosterone-secreted in renal tubular filtrate Potassium-hydrogen exchange

Back

Body is ___% fluid ____% intracellular ____% extracellular (can be measured)

Front

60% 2/3 intracellular 1/3 extracellular

Back

Coagulative Necrosis

Front

Occurs in heart, kidney, adrenal glands result of hypoxia protein denaturation occurrs; causes albumin to change to gelatinous state

Back

_________ accounts for 70% of capillary oncotic pressure

Front

Albumin

Back

Hypokalmeia

Front

Potassium Level less than 3.5 -Reduced potassium intake -Increased potassium into cells -alkalosis (K+ into cell) - insulin administration -GI vomit or diarrhea -kidneys secrete K+ to regulate Na+ (dehydration) Causes_____: Membrane hyperpolarization Neuromuscualr excitability decreases skeletal muscle weakness smooth muscle atony cardiac dysrhythmias flat T wave, low ST divot

Back

Greater of less for Arterial & Venous Net hydrostatic Net oncotic Net filtration

Front

Hydrostatic greater in arterial oncotic greater in venous Net positive in arterial, negative in venous

Back

ROS injury Alterations of proteins

Front

Causes fragmentation in polypeptide chains this causes pumps to fail, signaling to fail, and all cell processes to fail

Back

Results of Chronic cell injury

Front

Persistant stimuli response may involve only specific organelles or cytoskeleton phagocytosis of bac

Back

Hypokalemia Treatment

Front

Diet oral K+ 40-80 mEq/day IV No more than 20 mEq/ hour!

Back

Result of Autophagy cellular inury

Front

cell eats self

Back

Result of Accumulation/ Infiltration injury

Front

water, pigments, lipids, glycogen, proteins

Back

Hyperplasia

Front

Change in the number of cells, can be normal or abnormally shaped - compensatory hyperplasia: liver regrowth, callus formation -Hormonal Hyperplasia: ovulation w/ pregnancy leads to uterine hyperplasia & breast tissue enlargment -Pathologic hyperplasia: endometrial; imbalance of estrogen

Back

Gangrenous Necrosis

Front

Dry gangrene- from coagulative necrosis (hypoxia) Wet gangrene - develops as neutrophils invade the site and liquefy tissues

Back

What fluid compartments consist of intracellular fluid

Front

cells tissues

Back

Necrosis

Front

Cellular dissolution, rapid loss of plasma membrane organelle swelling, mitochondrial dysfunction -sum of cellular changes after cell death -5 types: fat, liquifactive, coagulative, caseous, gangrenous

Back

Mild hyperkalemia S&S

Front

Hyperpolarized membrane: causing neuromuscular irritability Tingling of lips and fingers restlessness intestinal cramping and diarrhea

Back

Metaplasia

Front

reversible replacement of one mature cell type by another less mature cell type - bronchial lining in response to smoking, newly formed cells do not secrete mucous or have cilia leading to a loss of viral protection

Back

2 types of chemical energy

Front

-Direct toxicity by combining w/ molecular component of cell membrane or organelles ex. cyanide inhibits mitochondria cytochrome oxidase and blocks electron transport -Indirect: most chemicals (drugs) not biologically active in parent form must be converted to reactive metabolite ex. Tylenol becomes a toxic metabolite in the liver

Back

2 defenses for chemical injury

Front

detoxification enzymes antioxidant system

Back

Chemical Injury

Front

-Electrophiles (electron lovers) are an atom or molecule that are attracted to electrons. They create a covalent bond which creates a fully charged center in molecules -Nucleophiles are atoms that donate an electron pair, are attracted to positive regions -The majority of chemical energies are electrophilic. The intermediates can interact w/ cellular macromolecules and can cause cell damage

Back

4 common themes in cellular injury

Front

1.ATP depletion 2. O2 and free radicals 3.Cellular self destruction 4. Defects in membrane permeability

Back

liquefactive necrosis

Front

Ischemic injury to neurons and glial cells generally in brain little connected tissue in brain digested leaving cysts

Back

Major intracellular cation and it's fucntion

Front

Potassium Neuromuscular excitability Acid/base balance

Back

Filtration forces

Front

capillary hydrostatic pressure and interstitial oncotic pressure

Back

Result of Necrosis cellular injury

Front

Severe cell swelling and break down of organelles

Back

Intracellular and Extracellular potassium limits

Front

Intracellular K+= 140-150 mEq/L Extracellular K+= 3.5-5 mEq/L

Back

Hypertrophy

Front

Cells get greater in size but keep their shape -heart stress will increase the size of the heart -muscle tension and stressing will cause growth of cardiac muscle

Back

Fat necrosis

Front

Lipases break down triglycerides, releasing fatty acids wich combine with calcium creating soaps breast tissue, and pancreas

Back

Hyperkalemia

Front

very rate Potassium level: greater than 5.5 (5 really but 5.5 is where a real concern happens) Pathophysiology: Hypopolarization=excitability Alters neuromuscular excitability people w/ renal disease can be hyperkalemic Causes of hyperkalemia: Increase intake penicillin, whole blood, K+ therapy, shifts of potassium from ICF, acidosis, Burns, crushing injury, sparing diuretics, low renal secretions, insulin defficiency

Back

How does K+ shift in and out of a cell

Front

Hydrogen-Potassium shifting In with insulin and beta antagonists out by hyperosmolarity, excersie, and cell lysis

Back

Result of cellular apoptosis injury

Front

Programmed cell death

Back

ROS from Reprofusion injury

Front

OH, O2-, H2O2 free radicals released causes further membrane damage and mitochondrial calcium overload can be reversed by antioxidant treatment (like vitamin C)

Back

ROS cell injury Lipid peroxidation

Front

destruction of unsaturated fatty acids, the double bonds are vulnerable to OH attacks Causes holes in cell walls, contents leak, cells pop

Back

Irreversible cellular injury results in

Front

"point of no return" Vacuolization of mitochondria influx of Ca++

Back

Filtration

Front

movement of fluid out of capillaries into interstitial space

Back

Reabsorption

Front

Movement of fluid into capillary space from interstitial space

Back

Necrosis vs. Apoptosis

Front

Apoptosis is programmed and can save some organelles to be used in other areas, where Necrosis saves nothing

Back

Reprofusion injury

Front

When cell's mitochondria try to resume ATP production after injury such as thrombosis. If you resupply O2, it can causes more damage. -broken mitochondria produces ROS when provided with O2 -ROS (or free radicals) are hazardous to the body - Complication of tissue transplant, myocardial infarction, stroke, renal hepatic cells

Back

Dysplasia

Front

abnormal development or growth of cells, tissues, or organs. Deranged cell growth (Atypical hyperplasia) - changes in cervical lining cells may lead to cancer -Strong indicator of breast cancer -If stimulus (like smoking) is removed, dysplasia is often reversed

Back

Section 2

(19 cards)

Action potential Hypokalemia & Hyperkalemia

Front

Hypokalemia: hyperpolarized, slow depolarization, membrane potential becomes more negative Hyperkalemia: hypopolarized, faster depolarization, if long term you decrease the ability to repolarize, requires less stimulus for action potential

Back

Hyperphospatemia

Front

levels greater than 4.5 mg/dL associate with Ca++ levels cell destruction intake of enemas or laxatives (these have a lot of phosphate in them) Treatment: dialysis and hydration aluminium hydroxide

Back

Hypercalcemia

Front

greater than 10.5 mg/dL ionized causes: increased bone reabsorption malignancies decrease phosphate levels hyperparathyroidism excess vitamin D Immobility Pathology: decreased neuromuscular excitability weakness CNS depression Shortened QT interval Impairs renal response to ADH

Back

Hypermagnesia

Front

greater than 2.5 Causes: Renal failure, magnesium containing antacids, administration, toxemia, premature labor is given IV magnesium to prevent labor Patho: slowed neuromuscualr activity lethargy drowsy respiratory depression Bradycardia hypotension Treatment: Dialysis

Back

Hypercalcemia S/S

Front

increases the block of Na+ into cell decreased neuromuscular excitability increased bone fractures Kidney stones Constipation

Back

Major intracellular cation 2nd most abundant

Front

Magnesium Plasma concentration is 1.8-2.4 mEq/L Required for ATPase activity Inversely related to potassium

Back

Hypocalcemia diagnosis and treatment

Front

Diagnosis: serum levels, increased neuromuscular excitability Treatment: Acute= emergency IV Chronic= supplements vitamin D

Back

Severe Hyperkalemia S&S

Front

-Cell is unable to repolarize -results in muscle weakness - loss of muscle tone -flaccid paralysis -cardiac arrest

Back

calcium and phosphate regulation

Front

Regulated y parathyroid hormone, Vit. D hormone, calcitonin hormone regulates these PTH- increases plasma calcium levels via bone reabsorption Vit D- fat soluble steroid that increases calcium absorption from the GI tract Calcitonin- decreases plasma calcium levels

Back

Calcium functions and type

Front

Protein bound Ionized (only kind we can use) Muscle contractions stored in bones 99% in bone blood clotting cardiac contraction nerve impulses

Back

Hypercalcemia Diagnosis and Treatment

Front

Diagnosis: clinical and lab results Treatment: rehydration increase urinary excretion decrease bone reabsorption

Back

Phosphate

Front

85% in bone creatine phosphate Ca++ and HPO4 concentration are rigidly controlled Ca++ x HPO4 = K+

Back

Hypocalcemia

Front

Ionized less than 4.0 mg/dL causes: abnormal renal loss mobilization from bones protein binding Chvotek's sign: touch cheek lip twithces Trosseaus sign: bp cuff greater than 200 causes hand tetany Patho: increased neuromuscular excitability membrane more permiable to Na+ Tetany seizures laryngospasms

Back

What regulates calcium

Front

Parathyroid glands renal tubules C cells of Thyroid gland

Back

Hypophosphatemia

Front

less than 2 mg/dL decrease GI absorption increases renal loss Pahto: oxygen transport energy metabolism leukocytes function poorly impaired clotting bone reabsorption CNS changes

Back

Hypocalcemia S/S

Front

C.A.T.S. C - Convulsions A- Arrhythmias T - Tetany (involuntary contraction of muscles) S - Spasms and stridor Decreases the block of Na+ movement across cell membranes increases neuromuscular excitability -distance between RMP and threshold decreased Muscle cramps: hyperreflexia, confsion, paresthesia

Back

calcium phosphate relationship

Front

calcium 8.5-10.5 phosphate 2.5-4.5 product <70 inverse relationship calcium up phosphate down calcium down phosphate up

Back

Magnesium levels and uses

Front

1.8-2.4 enzyme activation all activity using ATP DNA replication RNA translation Binds to calcium receptors

Back

Hypomagnesia

Front

less than 1.8 critically low less than 1.3 causes: malnutrition alcohol ingestion DM liver failure Drugs often with hypocalcemia or hypokalemia Pathology: increase neuromuscular excitability dsrhythmias paresthesias convulsions CV dysrhythmias Tetany

Back