Worksheetspathphysio 1 76-100
Total questions: 25
Worksheet time: 13mins
Patient I., 52 years old, was admitted with complaints of severe pains in the heart area, which do not subside from taking nitroglycerin, dizziness and sharp weakness. Objectively: the skin and visible mucous membranes are pale. The body temperature is 37.5°C. The boundaries of the heart are expanded to the left, the tones are deaf, the pulse is 100 min, low filling, irregular. Blood pressure is 95/70 mm Hg. In the lungs, wet wheezing is heard. A blood test revealed neutrophilic leukocytosis and an increase in ESR. What kind of syndrome can you think of?
reperfusion syndrome
resorption syndrome
the calcium paradox
oxygen paradox
myomalacia
A 63-year-old man suffering from bronchial asthma has been taking glucocorticoid medications for several years. During these years, body weight gradually increased, diabetes mellitus and hypertension developed. What is the pathogenesis of increased blood pressure in this patient?
reduction of ACE synthesis
reduction of sodium reabsorption in tubules
dystrophic changes in the renal tubules
increased angiotensinogen synthesis
reduction of adrenoreceptor density
Stress->increase in corticosteroid->increase in the synthesis of angiotensin converting enzyme angiotensinogen->? ->vasospasm->increase in TPVR->hypertension. The missing link in the pathogenesis of hypertension
increase water reabsorption in the kidneys
increased sensitivity to catecholamine’s vascular myositis
increase in the formation of angiotensin II
an increase in total peripheral vascular resistance
increased secretion of aldosterone
A common feature of chronic renal insufficiency, pheochromocytoma, Conn's syndrome, coarctation of the aorta, acromegaly is
hypotension
systemic vasculitis
venous thrombosis
hypertension
occlusive disease
Primary arterial hypertension can lead to
hypercortisolism
hyperthyroxine production
therosclerosis of the renal arteries
Chronic adrenal insufficiency
Frequent negative psycho-emotional stressors
The cause of left ventricular failure is
pulmonary emphysema
chronic pneumonia
bicuspid valve insufficiency
hypertension of the small circulatory system
tricuspid valve insufficiency
In the pathogenesis of secondary hypertension has a value
chronic emotional arousal centers
the excess production of adrenal hormones
persistent increase in excitability of sympathetic nerve centers
hereditary defect of membrane on pumps vascular myositis
reduction of inhibitory influence of the cortex on the vasomotor center
A clinical sign of right ventricular failure is
pulmonary edema
hepatomegaly
pulmonary hypertension
hemoptysis
expiratory dyspnea and hemoptysis
For the right heart failure is characterized
pulmonary edema
ascites
hemoptysis
cardiac asthma
hypertension pulmonary circulation
For the right heart failure is characterized by
hemoptysis
cardiac asthma
edema of the lower extremities
hypertension, pulmonary circulation
pulmonary edema
In the pathogenesis of deoxyhemoglobin in the blood increase in heart failure has value
acceleration of blood flow
increase in blood oxygenation in the lungs
an increase in blood oxygen capacity
decrease in tissue oxygen utilization
enhanced utilization of oxygen by tissue
For the right heart failure is characterized by
hemoptysis
cardiac asthma
hypertension of the large circulatory system
hypertension of the pulmonary circulation
pulmonary edema
Stress->increase in corticosteroid->increase in the synthesis of angiotensin converting enzyme and ? ->increase in the formation of angiotensin II ->vasospasm->increase in TPVR->hypertension. The missing link in the pathogenesis of hypertension
increase water reabsorption in the kidneys
increased sensitivity to catecholamine’s vascular myositis
increase in the synthesis of angiotensinogen
an increase in total peripheral vascular resistance
increased secretion of aldosterone
A 63-year-old man suffering from bronchial asthma has been taking glucocorticoid medications for several years. During these years, body weight gradually increased, diabetes mellitus and hypertension developed. What is the pathogenesis of increased blood pressure in this patient?
reduction of ACE synthesis
reduction of sodium reabsorption in tubules
dystrophic changes in the renal tubules
increase in the synthesis of angiotensin converting enzyme
reduction of adrenoreceptor density
A 42-year-old woman has persistent headaches, general weakness, muscle weakness, creeping sensation, polyuria, nocturia. The relative density of urine is 1001-1002. BP 230/120 mm Hg. Art. In the blood, the sodium content is increased and the potassium content is reduced. Ultrasound examination revealed a tumor of the right adrenal gland. What hormone does the tumor produce?
aldosterone
adrenalin
thyroxine
cortisol
norepinephrine
Through the axons, enter the central nervous system:
influenza A virus
streptococcal exotoxin
herpes viruses
pneumococci
adenovirus
The consequence of disinhibition syndrome can be:
development of dystrophic changes in neurons and innervated structures
development of organ atrophy
development of deafferentation syndrome
development of denervation syndrome
formation of a generator of pathologically increased excitation
A 25-year-old woman developed double vision and respiratory muscle dysfunction. Botulism was diagnosed. What is the most likely mechanism for the muscle dysfunction?
inhibition of glycine secretion into the synaptic cleft
inhibition of acetylcholine secretion into the synaptic cleft
inhibition of norepinephrine secretion into the synaptic cleft
blocking of glycine-sensitive receptors on the postsynaptic membrane
blocking of acetylcholine-sensitive receptors on the postsynaptic membrane
A 73 year old woman presented with muscle weakness and paresthesia in her arms and legs. Neurological examination revealed weakness of the flexors and extensors of the lower extremities, increased knee reflexes, and decreased vibration sensitivity. The patient most likely has a vitamin deficiency.
В1
В2
В6
В9
B12
In a 60-year-old man, in the early period after an acute cerebrovascular accident, the severity of neurological symptoms continued to increase, despite the restoration of blood flow in the damaged cerebral vessel. The cause of the worsening of neurological symptoms in the patient is:
decreased neuronal osmolarity
shrinkage of neurons
reperfusion of neurons
release of calcium from neurons
inhibition of glutamate receptors
A 28-year-old man has clonic seizures, twitching of the neck, face and trunk muscles with a short period of apnea, and foamy saliva coming out of the mouth. After the seizure, which lasts 2 minutes, the muscles relax. This typical form of pathology is based on:
decreased neuronal excitability
suppression of neuronal firing
destruction of dopamine neurons in the locus coeruleus
increased neuronal activity with hypersynchronous firing
predominance of cholinergic system activity in the striatum
Patient A., 72 years old, was admitted to the emergency room of the hospital complaining of weakness in the right half of the body. These symptoms appeared suddenly during a meal. The patient could not move his right arm and right leg, and speech difficulties (aphasia) developed. It is known from the anamnesis that the patient suffers from arterial hypertension, coronary heart disease, and has significantly elevated cholesterol levels. Upon examination: blood pressure 190/100 mm Hg, severe right-sided hemiparesis, positive Babinski reflex on the right. This condition is characterized by:
absence of tendon reflexes
appearance of pathological reflexes
muscle atrophy
muscle hypotonia
hypo-, areflexia
After a stroke, a 67-year-old man began to experience episodes of severe, difficult to bear polytopic pain, combined with vegetative and motor disorders. Most likely, the pathogenesis of these pains is due to:
suppression of brainstem excitability
formation of disinhibition syndrome in the thalamus
increased conductivity of nerve trunks
decreased excitability of the cerebral cortex
formation of GPUC in the spinal cord
Endogenous factors of damage to the nervous system are:
ionizing radiation
pesticides
lipid peroxidation products
ethyl alcohol
herpes virus
Neurogenic dystrophy is:
autoimmune brain damage
disruption of endorphin synthesis
disruption of metabolism in tissues with a disorder of their innervation
breakdown of higher nervous activity
parabiosis of nerve cells
