Pathophysiology Questions PDF
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This document presents a series of questions related to the field of pathophysiology. The material covers a range of topics pertinent to the study of this subject, including inflammation, metabolic disorders, and various disease mechanisms. The questions would provide a useful study resource for undergraduate medicine students.
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1- Which one is not a neurotransmitter? - glycine – inhibitory neurotransmitter - vasopressin - ADH - histamin – CNS transmetteur - thyroxine 2- What is the difference between Cushing disease and Cushing syndrome ? - Cushing disease is a pituitary adenoma provoking an ACTH hyper...
1- Which one is not a neurotransmitter? - glycine – inhibitory neurotransmitter - vasopressin - ADH - histamin – CNS transmetteur - thyroxine 2- What is the difference between Cushing disease and Cushing syndrome ? - Cushing disease is a pituitary adenoma provoking an ACTH hypersecretion - Cushing syndrom is an hyperadrenocorticism often due to cushing disease or other types of tumors 3- Which one is true ? - Meningitis causes hyperglycemia in CSF – causes hypoglycemia - Cellular edema can be caused by improper ADH secretion - Traumatic brain injury leads to vasogenic cerebral edema– osmotic cerebral edema , vasogenic is due to BBB injury 4- Antioxidants can be classified into extracellular and intracellular and enzymatic and non enzymatic according to their location and action 5- What are the 3 steps in neoplastic transformation ? - Initiation = Irreversible damage to DNA causes mutation - Promotion = Benign tumor formation - Progression = become malignant 6- What is true ? - TNF alpha is angiogenic– inflammatory mediators ( angiogenic factors are TGF, VEGF, PDGF, angiopoietin) - oncogenes induce apoptosis— promote growth ex : RAS or MYC - 2 more options 7- Diabetes insipidus definition : Diabetes insipidus is a condition in which the body produce too much urine and isn’t able to properly retain water. It is caused by a lack of ADH production (central) or a kidney cell resistance to ADH action (nephrotic) the origin can also be idiopathic. The clinical symptoms are polyuria, polydipsia, weight loss and neurological symptoms. 8-function of histamine and serotonin - Vasodilatation - Increased vascular permeability - Bronchoconstriction - Pain - Tachychardia - Activation of lymphocytes 9- On which cells are the adhesions molecules found ( 3) - Leukocytes - endothelium - platelets 10-What acid base balance disorder is caused by myocardial infarction ? - Metabolic acidosis 11- Which one is false ? -bicarbonate ion pass completely the nephron filtration - Bicarbonate ion is absorbed, H is excreted - Bicarbonate ion is reabsorbed, Na is excreted - Carbonic anhydride catalyzes carbonic acid formation in renal tubular cells 12- In which acid base balance vomiting is the cause and why ? -Metabolic alkalosis due to a loss of HCL ( acid)-- can also be due to sweating in horses or hyperaldosteronism ( increase K+ excretion) 13- Which are the characteristics of congenital hypothyreosis ? - it is secondary due to a TSH deficiency - it causes disproportionate dwarfism 14- What is insulin resistance and factors that causes it ? -It is when cells ( for exemple muscle, fat and liver) dont respong to insulin stimulation and therefore dont take in glucose - It can be caused by cushing syndrom, obesity, genetic predisposition, hypertension, chronic hyperinsulinemia, Ig against the insulin receptors, acromegaly 15- What is acromegaly and what causes it ? -hypersecretion of growth hormone after the closure of the epyphysis -origin can be a pituitary adenoma ( generally in old tom cats) or a hyperplasia of mammary gland ( in dog ) -symptoms are in dogs massive hypertrophy of the lips, of the pharynx, of the soft tissues, thick skin, polyuria, polydipsia, in cats it leads to obesity ( DM), and causes hyperglycemia 16- Describe clinical manifestation of cushing syndrome ? - Clinical signs of cushing syndrome are hypertension, hyperglycemia, increased level of blood cholesterol, abdominal distention, fragile and dry skin, dull hair, reproductive disorders, polyuria, polydipsia. In cats it can also cause some lethargy, obesity and skin infections. And in ferrets we can see some urination disturbance, aggressivity, swollen nipples and vulva. 17- Define inflammation and its goal ? - it is a protective response of vascularised tissue to an initial injury. It is also a fundamental homeostatic mechanism with the aim of diluting, isolating and remove the cause of the injury and repair the affected tissue - It is characterised by a cellular and vascular cascade events, with an increase number of cells, protein and fluid in the interstitial tissues. 18- What is SIRS and when it can develop ? - SIRS or systemic inflammatory response syndrome is an exaggerated defense response of the body to a stressor it can develop during sepsis, pancreatitis, trauma or severe bacterial infection 19- What are the possible outcome of inflammation? -Abcess -If acute it can lead to chronic inflammation -scar formation ( healing by fibrosis) - resolution 20- Define the term neoplasm - Neoplasm is an abnormal growth of cells in the body, it has no biological purposes, is irregular and disorganized and does not responde to the control mechanism of cell growth. it can be benign or malignant. 21- What are the main characteristics of malignant tumors ? - metastasis (spreading of the tumor) - invasion of nearby tissues - cells vary in size and shape - rapid growth - necrosis if poor blood supply - poorly differentiated morphological features - Anaplasia 22- Enlist causes of metabolic acidosis - ingestion of acid compounds - increased metabolic production of acid ( ruminal acidosis or ketosis or DM) - decreased H excretion and decreased bicarbonate reabsorption ( renal disease) - loss of base (diarrhea) 23- What is the principle of alkalosis treatment ? - Increase the acid uptake or decreasing the base level 24- How ROS act in physiological processes? -physio : help in cell growth, activation of receptors and protein synthesis, aid in gene expression - patho : oxidate molecule, impaired cell function and cell death, antimicrobial and cytotoxic action == oxidative stress 25- Consequences of oxidative lipid damages ? - changes in membrane permeability and fluidity, changes in cell integrity, generation of products of lipid peroxidation ( toxics) - 26- What causes myasthenia gravis and how does it manifests clinically ? - myasthenia gravis is caused by a production of antibodies towards the Ach receptors, preventing it from attaching and therefore from inbhiting the nerve impulse - mains symptoms are an rapid and intense fatigue, difficulty in holding the neck, tiredness in chewing, strabism, falling eyelid, disturbance in breathing 27- what are the causes of interstitial edema? -it is due to an impaired outflow of the CSF, sometime caused by meningitis, hydrocephalus or subarachnoid hemorrhage 28- What is the cause of puerperal paresis in cows ? -hypoparathyroidism due to an inadequate response of the bone tissue to PTH - it causes severe hypocalcemia, hypophosphatemia, muscular weakness and paresys 29- Which pathophysiological mechanism are included in hyperphosphatemia de? - excessive phosphate intake - Decreased phosphate excretion ( renal failure, hypoparathyroidism) - Phosphate shift from intracellular to extracellular space 30- Enlist consequences of Vitamin A toxicosis - it causes anorexia, thick skin, malformation, premature closure of physis in growing animals 31- What are pelagra (Black tongue) and how does it manifests? - pelagra is caused by vitamin B3 deficiency and manifest by sores in the mouth, diarrhea, dementia, vomiting and dermititis (3D) 32-Most important extracellular buffer -Bicarbonate buffer 33- Most important cause of hypoparathyroidism - injury to PT gland or removal of PT gland 35- What is insulinoma - Tumor of pancreatic Beta cells, causing a continuous production of insulin regardless of the blood glucose level 36- Endocrine disorders that causes nervous system disorders - hypoglycemia ( voir karine explication) 37-Ros are formed in anaerobic/ aerobic 38- What is not correct : - Malignant hypercalcemia is often in cats with neoplasia– in dogs, with Pituitary adenoma - TGF beta is angiogenic - yes - metaplasia is often epithelial - yes - lymphosarcoma can cause anemia- yes 39- What is true : - glial cells are cleaning the synaptic cleft - neurotransmitters are produced in the synaptic cleft - synapse is only in brain 40- what is true : - PTHrP is produced by lymphocytes (by malignant neoplasia - anal sac adenocarcinoma, lymphoma, sq c carcinoma) - - ??? 41-Definition and causes of hyperadrenocorticism -Also called Cushing syndrome- endocrinological disease caused by prolonged elevation of glucocorticoids conc in blood -overproduction of cortisol caused by either pituitary tumor or adrenal tumor -glucocorticoids 42-List Anabolic hormone -GH - insulin -estrogen - progesteron 43- What are the symptoms of adisson disease ? - hyponatremia( hypotension, bradycardia,hypovolemia) , hyperkalemia( impaired heart rate, muscle weakness), stress intolerance, hypoglycemia, inapetence 44- Hydrogen peroxide is free radical yes/ no ? 45- Exudate is composed of Leukocyte and proteins 46-Metabolic alkalosis compensatory mechanisms -decrease respiratory rate -buffer system -renal compensation ( decreased H excretion, increase bicar. excretion, decreased bicar. reab.) 47- What is true : - Carcinoma migrates through blood vessels– mainly sarcomas, carcinomas are through lymphatics 48- define oxidative stress Imbalance between ROS production and their safe removal by antioxidant 49- Antinflammatory effect of glucocorticoid (cortisol) - Cortisol stabilise the lysosomal membrane = it prevents release of proteolytic enzyme - decrease vascular permeability= prevent transudate and exudatre= no edema - decrease migration of neutrophils and macrophages = decrease released of inflammatory mediators. stabilises lysosomal membranes - decreases permeability of capillaries - decreases both migration of white blood cells into inflamed area and phagocytosis of damaged cells - suppresses immune system, lymphocyte reproduction decreases, reduced amounts of T cells and antibodies in the inflamed area (no promotion of inflammation process) 50- Why does pendulus abdomen develop in Cushing’s syndrom - due to intrabdominal fat accumulation, muscle wasting, hepatomegaly ( enlarged liver) 51- two ways of uncontrolled cell growth -Activation of oncogenes ( ex: RAS gene) - inactivation of Tumor Supressor genes ( Ex: P53) 52- Myxoedema and when does it occurs - in hypothyroidism, dermal and cutaneous edema caracterised by a deposition of protein and mucopolysaccarhide. It is generally located under the tongue, on the limbs, or in the larynx or pharynx. 53- Vascular phase of acute inflammation - vasodilatation - increased blood flow – transudate and leakage – edema - increased vasc perm - stasis of blood flow ( decrease blood flow) 54- congenital hypothyroidism - already described - 55- causes of hypocalcemia - hypoparathyroidism - kidney failure - injury - metabolic alkalosis - vitamin D deficiency 56- List catabolic hormones - Glucagon - cortisol - catecholamines 57. Mechanism of Leukocyte adhesion deficiency (LAD) -inherited genetic disorder, inability of leukocyte adhesion to vascular wall. -deficiency or failure in expression of AMS -increased leukocyte number in blood without ability to emigrate through capillary wall towards inflammatory site -consequences; repeated bacterial infection and severe inflammation -Human, dog (Irish setter) and cattle 58.Thyrotoxicosis (hyperthyroidism) causes -excess production of thyroid hormones triiodothyronine and thyroxine from abnormally functioning thyroid gland. -primary hyperthyroidism; pathology within thyroid gland -increased sensitivity of thyroid gland to stimulation of TSH -excessive synthesis of T3 and T4 -secondary hyperthyroidism; thyroid gland stimulated by excessive TSH in circulation 59. Pituitary dwarfism - hereditary -deficiency of growth hormone (GH) and other pituitary hormones -caused by atrophy and cystic degeneration of the anterior pituitary. - 2 to 5 months of age, affected animals show proportional growth retardation, a woolly coat, hair loss, hyperpigmentation, and skin peeling. -Reproductive issues arise due to disrupted gonadotropin (GN) secretion. -By 3 to 5 years, animals become hairless, dull, and underweight, experiencing progressive pituitary failure and kidney damage. 60. 3 endogenous causes of inflammation Newly formed molecules/antigens Oxidative stress Immune reactions 61. Insulinoma clinical signs - lethargy, seizures, loss of coordination 62. Pheochromocytoma signs - hypertension, palpitations, weight loss, acute blindness 63. Angiogenic factors- angiopoietin, TGF-beta, PDGF, VEGF 64. Causes of MODS/SIRS -Sepsis (severe infection) -Acute pancreatitis -Severe bacterial or viral infections -Trauma (major injuries) 65. Compensation of metabolic acidosis in order Early compensation - by the bicarbonate buffer system or respiratory system Long term compensation - renal compensation, Using the phosphate buffer system and ammonium buffer system (NH4+) 66. Hyperaldosteronism = metabolic alkalosis? 67. Incorrect answer→ astrocyte makes myelin 68.why inflammation only in vascularised tissue *Diabetes mellitus *BBB - def, consist of sempermeable highly selective border between bl and bran that filtrate solutes from bl. Allow o2, co2, gl and small mol to pass. consist of: endothelium, balsam mem, tight junction, astrocytes and foot *ROS and sources reactive o sp (HO, H2O2, O) - Endogenous sources: produced physiologically in the mitochondria during respiration (main ROS = superoxide) Electron transfer in mitochondria Exogenous sources = heavy metals, tobacco, smoke, xenobiotics, ionising radiation *mech of metastatic process 2 ways of uncontrolled cell growth Activation by oncogenes - cause uncontrolled cell growth and division which can result in malignant tumours. Mutations can cause the conversion of protooncogenes (which control cell growth) into oncogenes Inactivation by tumour suppressor genes (ex p53)- necessary for cell cycle regulation.They stop the cell cycle when genetic damage occurs and induce molecular repair mechanisms. If they defect is too large, cell repair or apoptosis occurs. Defects in this gene leads to a tumour