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MIK SK 1 FEVER, Anamnesis, 5130021054_Kamila Ni'ami Permatasari, Dr.dr…
MIK SK 1 FEVER
Pathophisiology of Fever
Starting from stimulation of white blood cells (monocytes, lymphocytes and neutrophils) by exogenous pyrogens in the form of toxins, inflammatory mediators or immune reactions.
These cells will release chemicals, known as endogenous pyrogens (IL-1, IL-6, TNF-α, and IFN).
Exogenous and endogenous pyrogens will stimulate the hypothalamic endothelium to form prostaglandins
The prostaglandins formed will then increase the thermostat benchmark in the thermoregulation center of the hypothalamus
The hypothalamus will consider the current temperature to be lower than the new benchmark temperature
so this is triggers the mechanisms to increase heat such as shivering, there will be an increase in heat production & a decrease in heat reduction which will ultimately cause the body temperature to rise to the new benchmark. And there was a fever.
Hepatitis C
Pathophisiology
3 Stages
The Icteric stage
Characterized by dark urine, the appearance of jaundice, clay-colored stools, and an enlarged liver
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Prodromal stage
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This body response is characterized by the appearance of symptoms such as fever, fatigue, nausea, vomiting, skin rashes and joint pain
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Pathogenesis
Immune Response
The immune system reacts to infection by creating an immune response. However, HCV has the ability to evade the immune system in several ways, allowing it to persist in the body for long periods of time.
Inflammation
An excessive immune response and chronic inflammation in the liver are the main features of hepatitis C. This can lead to hepatocyte damage and the formation of scar tissue (fibrosis).
Initial Infection
After entering the body, HCV targets hepatocytes, the main liver cells. The virus enters the hepatocytes and begins to replicate in them.
Progression to Cirrhosis
If HCV infection is left untreated, fibrosis can progress to cirrhosis, which is an advanced stage of liver damage. Cirrhosis can cause serious complications such as liver failure and liver cancer (hepatocellular carcinoma).
Transmission
HCV enters the human body through contact with infected blood, such as sharing needles among drug users, past unsafe blood transfusions, or unsterile medical practices.
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Hepatitis is inflammation of liver cells caused by various causes: Infection, drugs, alcohol, autoimmune disease, and metabolic disorders
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Preventive
Do not share personal items, because they are easily contaminated with blood
Ex: razors, toothbrushes & nail clippers
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Differential Diagnose
Hepatitis
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A (HAV) : RNA Virus
Anti HAV IgM (-),anti HAV IgG (+)
Anti HAV IgM (-),anti HAV IgG (+)
Anti HAV IgM (-),anti HAV IgG (+)
Anti HAV IgM (+), anti HAV IgG (-)
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E (HEV) : RNA Virus
Anti HAV IgM (-),anti HAV IgG (+)
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Bilirubin Metabolism
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Post-Hepatic
In the small intestine, and then released into some hydrolyzed bilirubin to produce unconjugated bilirubin and glucuronic acid.
Unconjugated bilirubin is reduced by colonic bacteria to stercobilinogen and urobilinogen,
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some is absorbed and returned to the liver for reconjugation (enterohepatic circulation) or otherwise excreted in the feces or urine.
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Anamnesis
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BP: 120/70 mmHg; Pulse: 80x/ min; RR: 18x/ min, T: 39°C
Serological Test: IgM HAV (-) IgG HAV (+), HbsAg (-), Anti HBC -, HCV RNA (+), Anti HCV (+)
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Dr.dr. Wiwik Winarningsih, MARS
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