Pathophysiology_FULL

duodenal reflex: decreased pH in antrum(2-2,5) or pH in duodenum (4)> decrease HCl secretion)

Mucus- gel like film about 1mm thick, consists of glycoproteins(NANA-Nacylneuraminic acid, fucose, bicorbonates keep stable pH 7on the epithelial cells while pH in. the lumen is 1,5 Prostaglandines E and F-stimulate mucus, glycoproteins, bicorbanates secretion; increase blood flow; increase hydrophobic properties of mucus

Complications: perforation>peritonitis; bleeding; obstruction by scarring

Therapy: diet; analgetics; blockers og H2histamine receptors, blockers of proton pump; antibiotics; protective drugs: polysaccharides and sulfur, Prgl E.

58. Acute liver insufficiency. Clinical symptoms and their pathogenesis.

Condition of the liver when it can not maintain homeostasis Symptoms:

headache, floaters in the eyes, weakness, depressed mood-astenovegetative syndrome(incr amount of toxins

Jaundice, incr amount of total bilirubin(hyperbilirubinemia)

hemorrhages on the skin and mucosa-Hemorrhagic syndrome(decr synthesis of clotting factors) nausia, vomitting, lack of appetite-Dyspeptic syndrome(intoxication and disorders of digestion) dark urine with production of foam when shalingcholemia

colorless fecesacholia

59. Syndromes of chronic hepatic failure Portal-to systemic shunting: clinical signs with their corresponding mechanisms.

Hepatocellular insufficiency( decreased. Metabolic, detox and barrier functions): Carb metabolismlow glycogen store>hypoglycemia, low glucuronic acid>inadequate detoxication

Protein metabolismlow albumins>edema, disproteinemia: decr alb/glob, incr ESR, incr A/A in blood and aminoaciduria, incr ammonium and decr urea because of decr synthesis, decr amount of clotting factors I,II,V,IX,X,XIII and hemorrhagic syndrome, low prothrombin index, decr synthesis of transferin to anemia, decr depo B12 to anemia;

Hormonal imbalance

Lipid metabolismdecr cholesterol and bile acids

Decr barier functions- infectious diseases, allergies, toxemia Hemorrhagic syndrome- decr synthesis of clotting factors Dyspeptic syndrome- intoxication and disorder of digestion

Portal hypertension- incr hydrostatic pressure in portal vein(suprahepatic block in right vent heart failure; intrahepatic block in cirrhosis; intrahepatic block). As a result of portal hypertension there are formed shunts portocaval: Capet Medusa, in esophagus, hemorrhoid veins. Symptoms of portal hypertension:

Hepatomegaly

Hepatosplenic syndromecommon blood and lymf outflow

Ascities-incr in hydrostatic pressure on venous end, decr oncotic pressure, incr lymf production till 20l a day, activation of RAAS and ADH

Shunting and varicous enlargement of veins> may lead to bleeding from that veins Intoxication and further dyspeptic syndrome and weight loss

60. Types of Jaundice. Intrahepatic form.The main causes and mechanism of this type of jaundice. Clinical and laboratory manifestations.

Suprahepatic( hemolytic) jaundice: incr UCB comes through the blood to liver and converted intoCB that later converted to UB and SB(hypercholic stool), dark urine( becouse of UB and SB from hemorrhoids), Large amount of UCB in the skin> lemon-yellow tint, in case of UCB >250mkmol/l- comes through hem.enc. barier(nuclear jaundice)>encephalopathy. Anemia Infrahepatic(mechanical) jaundice: no bile in the intestinum( acholia:colorless feces, steatorrhea and creatorrhea, meteorism, bacterial overgrowth, decr lipid sol vitamins) and regurgitation of bile and appearence of bile in the blood(cholemia). Incr CB(more 50%) and in

Anemia( decr erythropoietin synth)

bleeding tendencies, hemorrhagia, GI bleeding( impaired platlet formation) Arterial hypertension( activation of RAAS)

Edema( fluid retention and hypoalbuminemia)

Congestive heart failure, pulmonary edema( incr extracellular folume) Infections( impaired skin and mucosal barriers)

Peripherial neuropathy(uremic toxins> atrophy and demyelination of nerves) Lab signs of Uremia

Uremiasyndrome of body intoxication by uremic toxins, severe azotemia, hyperhydration, distorbances of electrolite balance, metabolic acidosis

Low pH(lower 7,35); blood urea nitrogen>30mmol/l, urea>6mmol/l, creatinine> 0,1mmol/l

63.UPPer and lower motoneurons injury Lower motoneurons injury

Causes: Poliomyelitis( motoneurons in anterior horn of spinal cord); Amyotrophic lateral sclerosis( glutamate leads to overirritation and death); injury of axon( distal axonopathy, wallerian degeneration); Botullinum toxin( no ACH release); Lambert-Eaton syndrome( IgG react with proteins on nerve terminals and damage them); Organophosphates( block of cholinesterase); Myasthenia gravis( IgG against Ach-receptors)

Symptoms: Flaccid paralysis No voluntary movement

No reflectory movement Atrophy

Fasciculation, fibrillation Hypotonia

Upper motoneurons injury

Causes: Parkinson’s disease (degeneration of dopaminergic neurons ); Huntington disease( degeneration of basal ganglia, putamen, degeneration of cholinergic and GABA neurons) Symptoms: Spastic paralysis

No voluntary movement Hypertonia Pathological reflexes No atrophy

64. Neurotransmission disorders

Botulism

toxin consist of heavy and light chains. two heavy chains forme a tunnel for light chain in the presynaptic membrane, light chain destroy anchor protein SNAP-25> vesicles with neurotransmitters cant attach to the membrane. No Ach release. Appears in about 6 hours after exposure.

Symptoms: vomiting, diarrhea, paresis of accommodation, muscular weakness. Further paralysis of somatic muscles( diplopia-double vision, dysphagia - disorder of swallow, dysphoniadisorder of speech; disorder of muscles of limbs and respiratory muscles) Therapy: anti botulinum serum, antibiotics, oxygen.

Myasthenia gravis

Appearance of Antibodies against Ach receptors. After attachment of IgG it leads to endocytosis of aggregated receptors and further lysosomal destruction> decr amount of Ach receptors followed by widened synaptic cleft.

Symptoms:muscle weakness, weakness of extraocular muscles. Therapy: blocker oa Ach-esterase, immunsupressors, corticosteroids

Organophosphate poison( clorophos, tabun, zarin, zoman)

it irreversible attaches to Ach esterase and blocks it, as a result accumulation of Ach in the cleft and irritation of muscarinic and nicotinic receptors

Symptoms

M-receptors: myosis, bronchospasm, vomiting, incr mucus production in bronchi N-receptors: fibrillation of muscles, incr AP

Therapy: drugs that destroy bands of esterase with poison, reversible inhibitors of esterase

65. Parkinson’s disease and Huntington’s disease

Parkinsonism

Degeneration of dopa neurons in substance nigra leads to increased inhibitory effect on thalamococrtical neurons that take part in motion control, besides lack of dopa neurons leads to free action of cholinergic neurons in striatum > tremor

Symptoms: akinesia, bradikineasia, rigidity, postural abnormalities(rigidity) Huntington

Degeneration of cholinergic and GABA neurons in Caudate and Putamen>decreased inhibitory effect

Symptoms: hyperkinesia, dementia

There is no specific treatment, use antidopaminergic drugs to decrease hyperkynesia

66. Pain

Pain is unpleasant sense, warning signal helps to protect the body from tissue damage. Types: physiologic(adequate reaction on dangerous situations and acts to warn about potential damage) and pathological(appears after damage);

Transitory pain(appears after even slight irritation of pain receptors and work as a warning), Acute(may be divided into localized and unlocalized) and Chronic;

?Nociceptive pain(irritation of nociceptors), neurogenic(damage of central or peripheries parts of neural system ), psychogenic.

Pain is transmitted by Aq fibers(acute, localized pain, make contact with neurons of dorsal horn I- II plates of Reksed) and C fibers(burning, bad localized, make contact in dorsal horn V-VII plates of Reksed) by glutamic and asp acids and sub P

Two main pathways: neo-spinothalamic(to ventro past nuclei of thalamus and then somatosensor zones of cortex S1,S2)and paleo-spinothalamic tracts(to reticular formation>post nuclei of thalamus>lymbic cortex-emotions)

Antinociceptive systems

Opiate system -presynaptyc inhibition by dinorphin, enkephalins, endorphin Adrenergic systempostsynaptic inhibiton

GABA system-