EXAM PATHOPHYSIOLOGY 2020/21

Illustration of human body systems in a medical context, emphasizing pathophysiology, with diagrams of inflammation, diabetes, and cardiovascular health

Pathophysiology Exam Quiz

Test your knowledge on pathophysiology with our comprehensive quiz designed for medical students and healthcare professionals. This quiz contains 28 questions covering various aspects of inflammation, diabetes, cardiovascular issues, and more.

  • Detailed questions on key pathophysiological concepts
  • Ideal for exam preparation and self-assessment
  • Gain insights into clinical implications in healthcare
28 Questions7 MinutesCreated by StudyingScience102
Damaging factors in inflammation:
Prostaglandin
NET
Cytokines
ROS
Indication for performing OGTT: know about impaired fasting glucose values, DM values
Fasting glucose 115 mg/dL and OGTT 180 mg/dL indicate DM
OGTT measurement of 150 mg/dL indicates Impaired fasting glucose
OGTT 180mg/dL indicates Diabetes
Directly after a meal, random glucose testing 210 mg/dL indicate DM
Mast cell releases
Arachidonic acid derivatives
Histamine
Complement
IgE
Increased permeability of the intestinal endothelium enables the absorption of:
Toxic agents
Antigens
Reabsorbed agents destroy the host tissue
Increased uptake of carbohydrates leading to type 2 diabetes
Movement of water in Fluid compartments:
Can be found predominantly in intracellular fluid space
Moves freely between all compartments described by universal rules
In order to be appropriately distributed – it requires energy
Transports predominantly dissolved substances
*Endothelium in inflammation:
Expresses on their membrane surfaces interleukins and selectins
Permits/ allows extravasation of leukocytes
Initiation of inflammation promoted by damage of endothelium
*Hypersensitivity types
Type IV develops very fast after initial infection
Type II is non-organ specific
Type I is “produced” by Th2
Type III can result into chronic inflammation
Compensation mechanisms
Respiratory acidosis compensation by retention of bicarbonate
Respiratory alkalosis compensation by excretion of bicarbonate
Metabolic alkalosis by Hypoventilation
Metabolic Acidosis by retention of CO2
Apoptosis which is NOT a morphological feature
Loss of membrane integrity
Shrinking of the cells
Apoptotic body formation
Caspase activation
Nucleus degraded late in process, caspases
*Complement in inflammation:
C5b67-chemotaxis
MAC complex
Activation of Mast cells
Opsonization for NK-cells in ADCC
Flow cytometry:
Laser light hits the cell flowing in the stream formed by the sheath fluid
There is a separate detector for each fluorescent channelt
A filter before a detector to reduce light
4 additional (detector) to the FSC and SCC
Neoplasms what causes
Mutations induced by chemical factors – oncogene
Mutations induced by physical factor by irradiation
Transformation of proto-oncogene to oncogene
Carcinogenesis by oncogenic virus
Man comes to the emergency room complaining of chest pain for 2h, not relieved by rest or sublingual NTG. Troponin is elevated 0.9ng/L. Based on this:
Very likely angina
Very likely MI
Very likely gastritis
Less likely angina
MI consequences:
Mitral valve regurgitation
ST depression in V1-3 precordial leads points to an anterolateral infarct
Skin discoloration due to jaundiced
Pain in the left arm and shoulder
Upper git bleeding:
Anemia
Hypovolemic shock
Fresh blood in stool
Hematemesis
Folic acid deficiency:
Congenital or acquired absence of intrinsic factor
Excessive ethanol intake
Inability to absorb properly
Intestinal polyp
Man with blood pressure 129/84- 139/89. Mean BP of 134/86 indicates which type of hypertension?
Normal/optimal
Prehypertension
Stage 1 hypertension
Stage 2 hypertension
*Primary mechanism in development of T2DM:
Insulin resistance
Beta cell defect
Immunoglobulins against beta cell
Immunoglobulins against insulin
Pulmonary disease with commonly fatal outcome:
Acute pneumonia due to viral infection
Pneumothorax-injury to lung
Hay-fever
Focal pneumonia causing bronchial obstruction
Stroke – typical symptoms:
Sudden problems with speaking
Dark skin due to activation of RAA system
Focal drop
Pain of lower body
Shock – non-progressive phase actions:
Increased in RAA system
Increase contractility
Increased Sympathetic system
Decreased CO
. Hypersensitivity reactions (cannot): macrophages which MHC to which cell
MHC I to Tc-cells
MHC I to NK cells
MHC II to Th-cells
MHC II to Tc-cells
Liver cirrhosis causes:
Hemorrhoids
Esophageal varices
Primary hypertension
Caput medusa of the head
Immunodeficiencies – lead to increase of following types of infections:
T-cells deficiency mainly fungi
B-cells deficiency fungi, viruses, bacteria
Complement deficiency mainly viruses
Phagocytes deficiency fungi and viruses
Indicate the potential mechanism of hypotensive effect after body weight normalization:
The decrease of peripheral tissue resistance for insulin in the body of obese person
The decrease of hyperinsulinemia state in the body of obese person
The increase of cardiac output in the body of obese person
The decrease of autonomic nervous system activity in the body of obese person
DM vascular effect complication
Ulceration of diabetes foot
Numbness of “fingers of foot” and foot
Constipation and vomiting
Risk factors for diabetes 2 + where you should perform OGTT:
Women with polycystic ovarian syndrome
Hypertension
TAG > 250 mg/dL
Obesity > 30
Patient with left sided heart failure – what can you expect/ what should you do:
Edema of lips and eyelids
Organomegaly
Elevation of jugular venous pressure
Congestion
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