Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
159 Cards in this Set
- Front
- Back
|
What is a subclinical state? |
Pathological changes have occurred but no manifestations |
|
|
5 main disciplines of pathophysiology |
Histopathology Haematology Chemical pathology Microbiology Immunopathology |
|
|
What is the normal range for specific gravity of urine? |
1.005-1.030 |
|
|
pH range of urine |
4.6-8.0 |
|
|
Failure to excrete N wastes will lead to what increased serum results?
|
High serum urea and creatinine |
|
|
What are the ranges for Anuria and Oliguria? |
Anuria 0-50ml/day Oliguria 50-500ml/day |
|
|
What is the effect of dehydration on specific gravity of urine? |
Dehydration increases specific gravity |
|
|
What is the effect on antidiuretic hormone on specific gravity of urine? |
Antidiuretic hormone causes H2O to be reabsorbed, preserving water in the body and yielding concentrated urine. Specific gravity will INCREASE. |
|
|
What is the effect of diabetes insipidus on urine specific gravity? |
Decreased s.g. due to low ADH -> fail to retain water, dilute urine. |
|
|
What is the normal range of protein concentration per dL in urine? |
< 10mg/100ml |
|
|
What does the presence of haemoglobin in urine indicate?
Bilirubin? Urobilinogen? |
Hb = RBC haemolysis Bilirubin = destruction of rbc and breakdown of haeme Urobilinogen = obstructive jaundice |
|
|
Nitrites in urine indicate what? |
Infection due to nitrite forming bacteria |
|
|
Differentiate transmembrane and peripheral proteins |
Transmembrane go through a membrane whereas peripheral are only bound to a single layer |
|
|
How hypoxic ischemic cell injuries work?
3 ways metabolically. |
Inadequate blood flow, hypoxia, ischemia, decreased mitochondrial oxygenation. Decreased ATP causes these effects: Increased glycolysis, decreasing pH, swelling, eventually autodigestion. Mitochondria swell and uptake calcium, damage. Na+ pumps fail, swelling, loss of enzymes, loss of protein synthesis |
|
|
If an adverse environment induces a cellular response that remains in homeostatic limits are the changes reversible or irreversible?
|
Reversible |
|
|
Cell injury is reversible if the nucleus ___ |
if the nucleus remains unscathed and the energy source is restored, or toxin neutralised. |
|
|
Genes are responsible for regular cell function and others are responsible for differentiation, which is most likely affected in adaptive cell changes? |
The differentiation genes |
|
|
What are some reasons for atrophy? |
Disuse Denervation Loss of endocrine stimulation Malnutrition Ischaemia or inadequate blood flow |
|
|
What are some ABNORMAL cases of hypertrophy? |
Left ventricular hypertrophy secondary to hypertension Kidney enlargement following nephrectomy |
|
|
What is a normal case of hyperplasia? Abnormal? |
Physiological breast enlargement in pregnancy Non-physiological benign prostatic hyperplasia due to hormonal stimulation, or warts due to virus |
|
|
Define metaplasia? How may it occur? |
Reversible change where on adult cell type is replaced with another. Stays within cell types, e.g. epithelial to other epithelial. May be due to undifferentiated stem cell changes. |
|
|
Define dysplasia |
Excessive cell growth of a specific tissue, bad shape and alignment. Often precedes cancer, but still reversible. |
|
|
What are 3 types of cell death? |
Pyknosis - irreversible condensation of chromatin in the nucleus. Karyorrhexis - fragmentation into nuclear dust Karyolysis - Dissolution of nuclear structure & lysis of chromatin |
|
|
How long before brain cells are irreversibly injured in hypoxia approximately? |
4-6mins |
|
|
What is the most likely mechanism behind skin damage? |
Reactive oxygen species and damage to melanin producing processes |
|
|
What is an inborn error of metabolism that causes abnormal intracellular accumulations of iron? |
Haemochromatosis |
|
|
Normal cell death is apoptosis, but what is abnormal cell death? |
Necrosis TYPES: coagulative liquefactive caseous fat gangrenous |
|
|
Coagulative necrosis is characteristic of which type of cell injury? (most common form of necrosis) |
Hypoxic |
|
|
Fat necrosis can happen after physical trauma to which organ/area? |
Pancreas, thus releasing lipases that attack nearby fat, fatty acids rapidly bind with calcium and make a soap |
|
|
Can ethanol be utilised directly by the muscle? |
No, liver first |
|
|
Why are women more susceptible to alcohol spreading? |
More body water space |
|
|
Healthy person clears alcohol at how many mg/100ml/hour? |
15mg/100ml/hour |
|
|
In alcohol dehydrogenase's first reaction, ethanol to acetaldehyde, what other product is made? |
NADH |
|
|
Acetaldehyde dehydrogenase yields what two products? |
Acetyl-CoA and NADH |
|
|
What is the fate of acetyl-coa from alcohol metabolism? |
Enter krebs cycle, locally or elsewhere. or fatty acid synthesis |
|
|
What is the MEOS pathway reaction? |
Ethanol to acetaldehyde consuming NADPH and O2, making NADP and 2H2O |
|
|
What does fatty liver occur in response to?
|
Increased synthesis of fat from accelerated Acetyl-CoA production |
|
|
What is the % chance of death within 4 years if scar tissue is present in the liver? |
50% |
|
|
What intermediate of alcohol metabolism causes cancer? |
Acetaldehyde |
|
|
What volumes of a) beer b) wine c) spirits are 1 standard drink? |
285ml beer - middy 100ml wine - less than half a glass 30ml spirit - small shot |
|
|
What % water is a newborn infant? Adult male? Adult female? |
Infant 75-80% Male 55-60% Female 50-55% |
|
|
What is the normal intracellular vs extracellular water distribution? |
Intracellular 65%
Extracellular 35% |
|
|
osmolarity can help determine if a solute will move across a membrane, whereas tonicity merely helps to determine where water will flow. true or false? |
True |
|
|
is HP > OP at the venous end? |
No. OP > HP at venous end, collecting water. |
|
|
increased capillary pressure, increased capillary permeability and obstructed lymph flow will have what effect on the body? |
Edema, compromised fluid return |
|
|
Why do wounds heal slower in those with edema? |
Compressed arteries reduce blood flow Poor capillary exchange reduces supply of nutrients for recovery and function |
|
|
Why would someone with nephrotic syndrome retain sodium and water? |
kidneys lose albumin, water follows, kidneys try to retain water through adh and aldosterone.
|
|
|
Why is skin breakdown common in edema? |
Poor circulation, weak skin prone to problems |
|
|
How much water do we lose in faeces, considering we excrete 8-10L into the GI tract? |
150-200ml normally. most reabsorbed |
|
|
Why does vomiting cause dehydration? |
Water lost from GI system, water moves to GI system from vasculature. |
|
|
What represents severe dehydration in adults? |
8% |
|
|
Why are elderly at risk of dehydration? |
Decreased thirst sensation |
|
|
Why are infants at risk of dehydration? |
Insensible losses Immature kidneys Higher metabolic rate Higher surface area to volume Higher relative water need and body % Inability to drink independently |
|
|
Define hypotonic dehydration |
Hypotonic dehydration is losing more electrolytes than water |
|
|
What change occurs in haematocrit in dehydrated people? |
Increase. due to rbc:volume ratio increasing |
|
|
What are the electrolyte and fluid losses from diarrhea and fever? |
Diarrhea: Water, Na+, K+, HCO3-, glucose Fever: Water, NaCl, CO2 |
|
|
What concentration is hypernatremia? |
145mmol/L,serum osmolality > 295mOsm/kg |
|
|
Causes of hypernatremia: MODEL |
Medications Osmotic Diuretics Diabetes insipidus Excessive H2O loss Low H2O intake |
|
|
Symptoms of hypernatremia: FRIED |
Fever Restless Increased BP Edema Decreased urine output or dry mouth |
|
|
Symptoms of hyponatremia:
|
Lethargy Confusion Weakness Decreased DTRs Postural hypotension Muscle twitching/convulsion Abdominal cramps and nausea |
|
|
Causes of hypochloremia: |
Vomiting lose HCL low intake or diuretics Cystic fibrosis |
|
|
Causes of hypokalemia: |
Diarrhea Diuretics excessive aldosterone or glucocorticoids - renal loss of K+ Alcoholism or starvation Treatment of DKA with insulin |
|
|
Hypokalemia symptoms: |
Neuromuscular dysfunction pins and needles loss of appetite weakness cardiac dysrhythmias |
|
|
Causes of hyperkalemia: |
Excessive oral intake renal failure aldosterone deficit potassium sparing diuretics crush injuries or burns severe acidosis |
|
|
Hyperkalemia effects: |
muscle weakness paralysis fatigue parasthesias cardiac dysrhythmias and arrest |
|
|
Hypomagnesemia causes: |
Renal losses Secretory diarrhea |
|
|
Hypomagnesemia effects:
|
Tachycardia weakness tetany |
|
|
Hypermagnesemia causes: |
renal failure medications |
|
|
Effects of hypermagnesemia: |
Weakness, nausea Impaired breathing Slow muscle and nerve conduction Bradycardia and arrythmia |
|
|
Hypocalcemia causes: |
hypoparathyroidism, hypomagnesemia vitamin d deficiency renal failure |
|
|
Hypocalcemia effects: |
Increased excitability arrythmias tetany convulsions and spasms |
|
|
Hypercalcemia causes: |
Increased bone resorption, incr PTH Immobilisation excess dietary intake of Ca or vit D |
|
|
Hypercalcemia effects: |
Decreased excitability Weakness Sluggish |
|
|
You consume cholesterol in food, what happens? |
Lipids emulsified by bile salts in small intense, packaged into fatty acid micelles, pancreatic lipase degrades the lipids, enter epithelial cells and form chylomicrons and return to liver via lacteals and lymphatic system. Cholesterol stays in chylomicron until remnant chylomicron is taken up by liver. Cholesterol can be used in VLDL or bile synthesis. |
|
|
Do we consume bad cholesterol in the diet? If not, why not? |
No we can't consume LDL in the diet. We consume certain lipids, e.g. most saturated fats and trans fats, that cause our body to synthesise more of its own LDL and thus there is a worsening of cholesterol secondary to these processes. But ultimately the body is in control of LDL levels. |
|
|
The liver has too much fat, i.e. TGs, what does it do? |
Large VLDL synthesis, ends up as sdLDL, very atherogenic. Excessive fatty acid flux causes this, e.g. diabetes uncontrolled. Risk of fatty liver due to FA storage in liver. |
|
|
Explain the reciprocal relationship between plasma HDL and plasma triglycerides |
|
|
|
Describe the various fates of triglyceride molecule when it leaves the liver |
VLDL -> IDL -> LDL VLDL travels to muscle and fat cells where TGs are removed. |
|
|
Why do pre menopausal women have favourable plasma lipid levels compared to men? |
Estrogen decrease LDL increase HDL Androgens opposite effect |
|
|
How can physical activity increase HDL cholesterol? |
Decreases TG levels by using them for aerobic metabolism Stimulate production of more HDL. Evidenced by studies on marathon runners. |
|
|
MM-LDL stimulates the endothelial cells to express what? |
Adhesion molecules such as X-LAM and V-CAM. |
|
|
What do adhesion molecules attract to the endothelial wall? What protein aids this process? |
Monocytes MCP-1 Monocyte chemotactic protein 1 |
|
|
The endothelial cells release a factor that acts on tissue bound monocytes, what is its name and function?
|
Macrophage Colony Stimulating Factor MCSF. It stimulates differentiation of tissue bound monocytes into tissue bound macrophages. |
|
|
MM-LDL in the arterial wall will run out of antioxidants, what will happen then? |
It becomes fully-oxidised LDL. Macrophages attack and engulf the oxLDL and prevent it from doing severe tissue damage. The macrophages release ROS which continues this cycle. |
|
|
What is a macrophage with lipid droplet accumulations called? |
Foam cell |
|
|
Foam cells release what enzymes? What do they do? |
MCP1, MCSF and interleukin-1 IL1. MCP1 attracts more monocytes. MCSF causes more monocyte differentiation. IL-1 together with MCSF stimulates smooth muscle cell proliferation around the foam cells including into the intima. |
|
|
When smooth muscle cells migrate from both sides of a fatty streak and encase the foam cells, what is it called? |
Atherosclerotic plaque |
|
|
Which connective tissue deposited in the smooth muscle tissue will reduce the flexibility of the arterial wall? |
Collagen deposition |
|
|
What are the functions of nitric oxide in blood vessels? |
Decrease leukocyte adhesion, decrease V-CAM I-CAM, inhibit MCP-1 Decrease endothelial permeability Decrease vascular smooth muscle cell proliferation Prevent platelet aggregation and clotting |
|
|
What effects do omega 3s have on blood, cardiac and lipoprotein areas? |
Lowers blood pressure - increased NO, increased membrane fluidity Reduce arrythmia Reduce cardiac death Lowers VLDL synthesis and increases LPL activity. |
|
|
What genetic variations reduce risk of CHD? |
High HDL levels CETP not functioning |
|
|
In anemia define 'chromic' and 'cytic' |
Cytic = size chromic = Hb concentration |
|
|
3 ways we can have anemia: |
reduced number of RBCs
decreased quality of Hb decreased quantity of Hb |
|
|
3 causes of anemia, broadly: |
blood loss impaired erythropoiesis increased rbc destruction |
|
|
Severe anemia involves dyspnea at rest, why? |
Hypoxia even at rest, compensations aren't enough |
|
|
Define: PCV MCV MCH MCHC RDW MPV |
Packed cell volume - Hct Mean cell volume mean cell hb mean cell hb concentration red cell distribution width mean platelet volume |
|
|
Define anisocytosis poikilocytosis |
Slightly uneven size uneven shape |
|
|
Name 2 macrocytic normochromic anemias |
Pernicious (b12) Folate deficiency anemia |
|
|
3 types of Microcytic hypochromic anemia |
iron deficiency sideroblastic thalassemia |
|
|
5 normocytic normochromic anemias |
aplastic anemia post-hemorrhagic anemia haemolytic anemia anemia of chronic inflammation sickle cell anemia |
|
|
In macrocytic anemia is Hb concentration normal? What about total Hb weight? |
Concentration normal total hb high |
|
|
How can we lack intrinsic factor? |
autoimmune reaction against parietal cells or IF interference of other autoimmune diseases surgery of gi tract aging |
|
|
Schilling test tests the absorption of what? |
Vitamin B12 |
|
|
Treatment of pernicious anemia? |
Injections of B12 |
|
|
What is the key difference in symptoms between pernicious and folate deficiency anemia? |
No neurological abnormalities |
|
|
Why are RBCs in folate deficient anemia megaloblastic? |
They can't divide because activated folate is crucial in their cell division |
|
|
If transferrin saturation is normally 30% but is now 15% or lower, what condition is likely? |
Iron deficiency |
|
|
The body contains approx __g of iron, 70% of which is bound to Hb |
5g |
|
|
Iron is stored bound to _____ and as _____ |
bound to ferritin haemosiderin |
|
|
how much iorn is lost per day? how much are menstrual cycle losses? |
1mg/day 20mg/month |
|
|
Which form of anemia is extremely common around the world? |
Iron deficiency |
|
|
3 stages of iron deficiency anemia development: |
1. body iron stores depleted 2. insufficient iron transported to marrow 3. iron deficiency anemia |
|
|
What is enteritis? |
Inflammatory process of the small intestine |
|
|
What does tropical sprue impair? What is the treatment |
Absorption of nutrients in intestine Supportive, electrolytes, antibiotics |
|
|
Celiac disease involves a loss of what structure? |
Mature villous epithelium |
|
|
Which part of gluten is toxic to celiacs? |
Soluble gliadins |
|
|
After gluten free diet how long til celiac symptoms disappear? Low long until atrophied villi heal? |
4 weeks 3.8 years |
|
|
What are some stimuli for irritable bowel syndrome? |
Stress, altered intestinal motility |
|
|
Does IBS have concrete structural or biochemical abnormalities? |
No it does not |
|
|
Crohn's Disease is an inflammatory disorder of: small, large or both intestines? |
Both |
|
|
What is a serious complication of crohn's disease? |
Intestinal obstruction and fistula formation. it fuses with other parts of intestine or bladder, urethra, skin etc. |
|
|
Treatment of crohn's? |
Antiinflammatory drugs surgical resection fish oil supplements |
|
|
Ulcerative colitis is characterised by what? |
Frequent watery stools Bloody diarrhea 30-40 times per day! Cause unknown Common bowel cancer |
|
|
Treatment of ulcerative colitis? |
Anti-inflammatories Surgery |
|
|
Diverticula are any sac or pouch formed by herniation of intestinal wall. What is difference between diverticulosis and diverticulitis? |
Diverticulosis: Presence of several diverticula Diverticulitis: Inflammation of diverticula especially colon. |
|
|
What % of diverticular disease cases involve sigmoid colon hypertrophy? |
95% |
|
|
Treatment of diverticular disease? |
nil by mouth, IV fluids -> bowel rest gradually back to high fibre diet |
|
|
Haemorrhoids are what? |
Swollen inflamed veins around the anus or rectum. |
|
|
Name 3 good bacteria in GI tract: |
Bifidobacteria E. Coli Lactobacilli |
|
|
Name 3 bad bacteria in GI tract: |
Campylobacter Enterococcus faecalis Clostridium dificile |
|
|
Non digestible fibre is fermented into what by gut microbiota? |
Short chain fatty acids: acetate, propionate, butyrate |
|
|
Which short chain fatty acid feeds other bacteria mainly? |
Acetate |
|
|
Can bacteria possibly synthesise B and K vitamins? |
Yes |
|
|
Bacteroidetes are associated with what body type? |
Lean body type |
|
|
Firmicutes are relatively higher in western countries true or false? |
True |
|
|
Akkermansia muciniphila may reduce what 3 conditions? |
obesity diabeetus inflammation |
|
|
Bifidobacterium has what effect on the gut mucosal barrier? |
It improves it, helpful for ulcerative colitis treatment |
|
|
Lactobacillus does what primarily? |
Protects host against pathogens |
|
|
E. coli does what to other bacteria? |
Keeps bad bacteria levels down |
|
|
Campylobacter infection usually occurs through which medium? |
contaminated food |
|
|
Enterococcus faecalis is a common cause of infections in which scenario? |
Post-surgical |
|
|
Clostridium dificile tends to appear most at what time? |
After a course of antibiotics when it can proliferate |
|
|
Akkermansia is often found in what common prebiotic sources? |
Grapes, pomegranate, cranberries |
|
|
Bifidobacterium is the bacteria found in ... |
probiotics, fermented foods |
|
|
Lactobacillus is in what products? |
Probiotics, yoghurt, kefir, buttermilk etc |
|
|
Define prebiotics and probiotics |
Prebiotics promote growth of bacteria in intestines Probiotics actually contain microorganisms |
|
|
Garlic and onions are examples of PRE or PRO biotics? |
Prebiotics |
|
|
Proton pump inhibitors favour growth of what bacteria? |
Streptococcus |
|
|
What can the gut influence on the gut brain axis? |
Neurotransmitters Stress Mood Behaviour |
|
|
Vagus nerve has many afferent fibres in the gut, what compounds are released by bacteria that may act on nerves? |
GABA, serotonin, dopamine, Ach etc |
|
|
Short chain fatty acids activate what nerve fibres? |
Vagus afferent fibres |
|
|
Reduction in vagal tone was found in what bowel diseases? |
IBD IBS |
|
|
Microbes help maintain cell-cell junctions in the gut and prevent leakages T or F? |
True |
|
|
Can gut microbiota decrease BBB permeability? |
Yes they can |
|
|
What pathways of communcation do we have gut-brain |
Neuroendocrine Enterochromaffin cells Neuroimmune signals Direct neural signals |
|
|
Whats the point of a fecal microbiota transplant? FMT |
restoration of microflora |
|
|
Faecal enemas are ___% effective in C. difficile cases that were antibiotic resistant? |
90% effective |
|
|
Can rat obesity be modulated through FMT? |
Yes normal rats can be made obese and obese rats can be made thin FMT from fat human makes mouse fat Thin human fmt makes fat rat less fat |
|
|
Human to human FMT can improve insulin sensitivity true or false?
|
True |
