Liver, Biliary And Pancreatic conditions, Signs, Causes And Differentials Flashcards by XXXXX XXXX | Brainscape

Q

What are the two classifications of conjugated hyperbilirubinaemia? (Not unconjugated, which is prehepatic)

A

Hepatocellular

Obstructive

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Q

What are the causes of obstructive jaundice?

A

Carcinoma of the pancreas head

Cholangiocarcinoma

Gallstones in duct* (or cholangitis/cholecystitis could cause this)

Sclerosing cholangitis

Lymph node metastases

Chronic pancreatitis

*stones in gall bladder cause no obstruction

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Q

Why does obstructive jaundice cause prolonged PT and APTT?

A

Obstruction of flow of bile causes reduced absorption of the fat soluble vitamins: D, E, A, K

Vitamin K is essential for the production of factors 2, 7, 9 and 10

When these factors aren’t produced, the intrinsic and Extrinsic coagulation mechanisms are inhibited, therefore bleeding time goes up

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Q

What are the causes of hepatocellular jaundice?

A

Viral hepatitis

Alcoholic hepatitis

Cirrhosis

Drug induced hepatocellular damage

Non-alcoholic fatty liver disease

Wilson’s disease (excess copper deposition)

Haemochromatosis (iron overload)

Autoimmune hepatitis

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Q

What are differentials for Jaundice with abdominal pain?

A

Cholangitis (RUQ pain + fever)

Pancreatitis (Epigastric pain radiating to back)

Gallstones (RUQ pain + fever)

Or gallstones in the bile duct (Epigastric pain radiating to back)

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Q

First thing you should think about in the case of jaundice with no abdominal pain?

A

Cancer of the pancreas, or liver, or anywhere in the biliary tree

Cholangiocarcinoma
Hepatocellular carcinoma
Hepatoblastoma
Cancer of the head of the pancreas

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Q

Signs of hepatobiliarypancreatic cancer?

A

Unintentional weight loss

Cachexia

Hard lymphadenopathy

Craggy liver edge

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Q

What are the four main cancers of the biliary system?

A

Carcinoma of the head of the pancreas (most common)

Primary hepatocellular carcinoma

Liver cancer as a metastasis

Cholangiocarcinoma

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Q

What are the signs of alcohol poisoning?

A

Confusion

Vomiting

Loss of coordination

Stupor (unresponsive)

Hypothermia

Bradypnoea

Seizures

Cyanosis

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Q

What is delirium tremens?

A

An acute confusional state due to stopping a chronic drinking habit (alcohol withdrawal), the worst presentation of alcohol withdrawal syndrome.

Characterised by signs of overactivity in the SNS.

Caused by abrupt decrease in ethanol level causing an imbalance of excitatory signals in CNS.

The NMDA receptors were upregulated and the GABA receptors downregulated during alcoholism, since alcohol did the work of the inhibitory pathways.

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Q

What are the signs of delirium tremens?

A

Confusion

Tremor

Anxiousness

HTN

Tachycardia

Insomnia

Irritability

Diaphoresis (sweating)

Headache

Hallucination

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Q

How long must you have the signs of liver inflammation to be diagnosed with chronic hepatitis?

A

6 months

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Q

What signs are specific to obstructive causes of hyperbilirubinaemia?

A

Pale stools
(no secretion in to bowel via biliary tree so no urobilinogen formed and so no stercobilogen production)

Dark urine
(increased bilirubin excreted, no urobilinogen)

Itching
(Associated with obstructive jaundice)

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Q

What is cirrhosis?

A

Fibrotic irreversible liver damage with regenerative nodules surrounded by fibrotic proteins.

Activation of stellate cells.
Loss of vitamin A
Production of TGF-Beta
- collagen formation occurs

Scar tissue builds up
Compression of sinusoids, portal veins and hepatic arteries
- portal hypertension
- liver has lost functional units
-decreased detoxification ability

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Q

What are the signs of acute hepatitis?

A

Malaise

Jaundice

RUQ pain (inflamed liver presses on Gleason’s capsule)

Severe acute hepatitis:

Confusion

Coagulopathy (increased INR and falling albumin indicates function is failing)

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Q

What are the signs of chronic liver disease?

A

Jaundice

Hepatomegaly

Spider naevi

Palmar erythema

Portal hypertension

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Q

In a patient who begins drinking, which disease states can their liver go through before cirrhosis?

A

Normal liver > Fatty liver > Steatohepatitis > Alcoholic hepatitis > Cirrhosis

Or patient can go directly:

Normal liver > Alcoholic hepatitis > Cirrhosis

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Q

What is a fatty liver?

A

An inflamed liver, due to proinflammatory effects of viruses, drugs, alcohol and other causes.

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Q

What is steatohepatitis?

A

An inflamed liver with fibrous tissue laid down within it. (Like a pre-scar)

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Q

What are the symptoms of compensated cirrhosis?

A

Can be asymptomatic for up to ten years

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Q

What are the causes of haemolytic jaundice?

A

Sickle cell anaemia

Incompatible blood transfusion (immune attack)

Hypersplenism (overactive spleen, not the same as splenomegaly)

Drug reactions

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Q

Which liver enzyme is saturated in haemolytic jaundice?

A

Glucoronyl transferase

Glucoronyl transferase only reaches peak function at 40 weeks gestation.

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Q

Which two symptoms distinguishes haemolytic jaundice and obstructive jaundice?

A

Dark stools and normal urine = Haemolytic
White stools and dark urine = Obstructive

Excess unconjugated bilirubin in serum can’t enter urine unless they are conjugated: unconjugated bilirubin is NOT water soluble.

Dark stools occurs because the GT enzyme is fully saturated due to excess unconjugated bilirubin, therefore max stercobilinogen present.

If obstruction occurs conjugated bilirubin enters blood and darkens urine, but cannot enter intestine to colour stools.

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Q

Which will rise in obstructive jaundice: ALP or ALT/AST?

A

ALP rises (ALT and AST will rise too but less than the rise in ALP)

The cystic/bile ducts are the bigger source of ALP

The liver itself is the biggest source of ALT/AST because they are conjugation enzymes

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Q

What is neonatal jaundice?

A

A very common condition (2/3 of all term babies, and 4/5 of all preterm)

Caused by low GT liver enzyme function.

Glucoronyl transferase only reaches peak function at 40 weeks gestation.

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Q

What is kernicterus?

A

Toxic yellowing of the brain.

Caused by unconjugated bilirubin crossing the BBB.

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Q

What signs and symptoms should you look for in a patient presenting with jaundice?

A

Presence of pain

Duration and any fluctuation

Scratches (itching from hyperbilirubinaemia)

Colour of urine and stools

Weight loss

Troisiers node (left supraclavicular)

Organomegaly

Fever

Spider naevi (oestrogen, non-blanching)

Palmar erythema (oestrogen)

Portal hypertension (Caput medusa, oesophageal/rectal varices)

Ascites (low albumin and portal hypertension)

Flapping tremor (encephalopathy)

Confusion (encephalopathy)

Vomiting (encephalopathy)

Fits (encephalopathy)

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Q

In a patient presenting with RUQ pain, which parts of their anatomy could be the cause?

A

Liver

Diaphragm

Gall bladder

Kidney

Bile duct

Duodenum

Pancreas

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Q

What are the differentials for RUQ pain?

A

Acute pancreatitis

Perforated viscera

Cholangitis/biliary colic

Pyelonephritis/renal colic

Acute mesenteric ischemia (emboli or thrombus)

Pneumonia

MI

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Q

What are the causes of hepatic encephalopathy?

A

Alcohol (binge drinking or quitting drinking)

Opioids

GI haemorrhage (causes increased ammonia production)

Increased protein intake (causes increased ammonia production)

Hypoglycaemia

Renal failure

Infection

Constipation

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Q

How is hepatitis A spread?

A

Faecal-oral spread

Associated with high risk countries and poor hygiene.

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Q

How is hepatitis B spread?

A

Blood

Sex

Maternal transmission

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Q

How is hepatitis C spread?

A

Blood (most common)

Sex

Maternal transmission

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Q

What are the risk factors for hepatitis B infection?

A

IVDU

Medical treatment with contaminated equipment

Maternal infection

Travel to Africa and Asia

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Q

What are the risk factors for hepatitis C infection?

A

IVDU

Medical treatment with unhygienic equipment

Tattoos

Sharing razors or toothbrushes

Q

Who is more likely to develop chronic hepatitis B infection, a newborn or a 5 year old ?

A

The newborn.

< 1 years old = 90% chance of chronicity

5+ years old = 1-5% chance of chronicity

Q

How is hepatitis E spread?

A

Faecal-oral route

Q

How is hepatitis A spread?

A

Faecal-oral spread

Associated with high risk countries and poor hygiene.

Q

How is hepatitis B spread?

A

Blood

Sex

Maternal transmission

Q

How does hepatitis C normally present?

A

Asymptomatic (there is no fulminant stage)

Later in life as cirrhosis

Q

What are the portal hypertension signs of cirrhosis?

A

Most often ASYMPTOMATIC

Portal hypertension:

Caput medusa
Ascites
Piles
Splenomegaly
Encephalopathy (less blood through liver means less toxins removed)
Renal failure (reduced return to kidney meaning RAAS system will constrict eff arteriolar and caused acute kidney injury)

Q

What are the hepatic dysfunction signs of cirrhosis?

A

Hepatic dysfunction:
1. Jaundice

Decreased drug metabolism (increased effects)
Atrophic testes and body hair loss (Decreased hepatic hormone production/metabolism)
Palmar erythema, Spider naevi and gynaecomastia (increased oestrogen)
Bruising (coagulopathy)
Hypoalbuminaemia
Leukonychia (hypoalbuminaemia)
Clubbing (any fibrotic change in body does this)
Dupuytren’s contracture (signs of alcohol excess)
Xanthelasma (sign of lipid disregulation)
Hepatomegaly (initially, then in later stages the liver shrinks)
Asterixis (encephalopathy)

Q

What are the signs of hepatic failure?

A

Bruising and spontaneous haemorrhaging (Coagulopathy)

Confusion and coma (encephalopathy)

Oedema (hypoalbuminaemia)

Increased sepsis risk (liver lymphoid function is normally very important)

Hypoglycaemia (no glycogen storage in liver)

Spontaneous bacterial peritonitis

Q

What are the signs of alcohol withdrawal syndrome?

AWS, Not delirium tremens

A

Tachycardia

Hypotension

Tremor

Confusion

Fits

Hallucinations

Nausea and vomiting

Q

What are the signs of delirium tremens?

A

Severe confusion

Agitation

Irritability

Seizures

Hallucinations

Mood changes (depression, anxiety)

Restlessness

Stupor

Fatigue

Insomnia or fatigue

Sensitivity to light, touch or sound

Body tremors

Q

How long after the final drink do the signs of alcohol withdrawal syndrome (or delirium tremens) begin?

A

10 to 72 hours after the final drink

Q

What are the infective causes of acute hepatitis?

A

Hepatitis viruses A, B and E

Epstein-Barr virus

Cytomegalovirus

Q

What are the main lifestyle factors that contribute to acute hepatitis?

A

Obesity

Diabetes mellitus

Alcohol excess

Q

Which drugs can cause acute hepatitis?

A

Antiepileptics

Rifampicin (antibiotic)

Flucloxacillin

Methotrexate

Paracetamol (as o/d)

Q

What are the autoimmune causes of acute hepatitis?

A

Autoimmune hepatitis (a condition where the liver’s own immune system attacks itself)

Primary biliary cholangitis

Primary sclerosing cholangitis

Q

What are the hereditary causes of acute hepatitis?

A

Hereditary haemachromatosis

Wilson’s disease

Alpha-1 antitrypsin deficiency

Q

How does alcohol cause alcoholic liver disease to occur?

A

Increased acetaldehyde (causes inflammation)

Upregulates P4502E1 (produces ROS > necrosis)

Increased hepatic macrophage activity (produces ROS > necrosis)

Inhibition of gluconeogenesis by NADH (due to NADH byproduct of ethanol conversion to acetaldehyde), and subsequent fatty acid oxidation, freeing fatty acids that infiltrate the liver

Q

What are the signs of alcoholic liver disease?

A

Common:
RUQ pain

Hepatomegaly

Haematemesis

Ascites

Weight change

Anorexia

Fatigue

Uncommon:
Melaena

Splenomegaly

Jaundice

Palmar erythema

Asterixis

Q

What is acute pancreatitis?

A

Sudden inflammation of the pancreas that is self-limiting and reversible.

MOA: zymogen granules activate before exiting the pancreas and autodigest the organ.

Q

What are the risk factors for acute pancreatitis?

A

Heavy alcohol use

Gallstones

Abdominal trauma

Steroids

Infections

Tumours

High triglycerides

Hypercalcemia

Q

What are the three main causes of acute pancreatitis?

A

Alcohol (40%)

Gallstones (40%)

Idiopathic

Other: trauma, steroids, mumps, autoimmune, scorpion/spider venom, Hyper-lipidemia/calcemia/parathyroidism, ERCP, drugs

Q

What are the signs of acute pancreatitis?

A

Sudden epigastric pain radiating to back (can be in hypochondriac regions)

Episodic

Nausea

Vomiting

Tachycardia

Q

What is chronic pancreatitis?

A

Recurrent/persistent, progressive injury to the pancreas with associated abdominal pain.

MOA: Inflammation causes scarring and loss of pancreas function.

e.g. alcohol damages acinar cells causing inflammation and membrane destruction, leading to pancreatic calcifications

Q

What are the threetypes of chronic pancreatitis according to the Sarles classification?

A

Obstructive pancreatitis

Inflammatory pancreatitis

Lithogenic or calcifying chronic pancreatitis.

Q

What are the signs of chronic pancreatitis?

A

Sudden epigastric pain radiating to back (can be in hypochondriac regions)

Episodic

Nausea

Vomiting

Tachycardia

Steatorrhoea

Brittle diabetes

Weight loss

Bloating

Q

What can cause decompensation of a stable liver cirrhosis?

A

Hypoglycaemia

GI bleed

Infection

Alcoholic binge

Q

What is diabetes mellitus?

A

Reduction in insulin action sufficient to cause a level of hyperglycaemia that over time, will result in diabetes specific microvascular pathology of the eyes, kidneys and nerves.

Oral glucose test = >11.1 mol/L

Or, Fasting glucose = >7 mol/L

Q

What is non-diabetic hyperglycaemia?

A

Insulin action is reduced such that blood glucose is raised but not to a level that will cause microvascular damage.

Oral glucose test = 7.8-11.1 mol/L

(AKA: prediabetes, impaired glucose tolerance, impaired fasting glucose)

Q

At what age is diabetes onset most likely type 2 than type 2?

A

Age 30 (after this, it’s more likely T2)

Q

How does diabetes type 2 originate?

A

Pretty much it’s fats making the liver and pancreas not store glucose and create insulin at the right moment.

Positive calorie diet
Increased VLDL triglycerides
Storage of fat in liver = Resistence to insulin suppression of hepatic glucose production = increased glucose production
Deposition of fat in islet cells = affects glucose sensing equipment = Decreased insulin release in response to food
Increased basal plasma glucose = increased basal insulin release - peaks in prediabetes stage

Q

Other than type 1 and 2, what other types of diabetes mellitus are there?

A

Maturity onset diabetes mellitus if the youth (MODY)

Exocrine pancreas disease - DM due to pancreatitis

Endocrinopathies - Cushing

Drug induced - antipsychotics and corticosteroids

Post-transplant

Q

Which sensation is lost in peripheral neuropathy before all others?

A

Vibration

Q

What are the three components of metabolic syndrome?

A

Central obesity

Diabetes mellitus

Hypertension

Q

What are the signs of diabetic ketoacidosis/hyperosmolar hyperglycaemic state?

(Same signs in both)

A

Signs of diabetes: polyuria, polyphagia, polydipsia, weight loss, weakness, sunken eyes

Hyperventilation (respiratory compensation)

Nausea and Vomiting

Abdominal pain

Dehydration

Hypotension

Decreased GCS

On investigation:
Hyperkalemia
Glycosuria (or ketonuria DKA)
Leucocytosis
Hyperlipidaemia
Raised creatinine

Q

How does diabetic ketoacidosis happen? What is the physiological process?

A

Decreased insulin means that the catabolic effects of other hormones (glucagon etc) aren’t balanced out
Therefore glucose levels build even higher but the body cannot use them without insulin.
The liver begins to break down fats to form free fatty acids, this generates ketones
Ketones are acidic, so this produces a metabolic acidosis

Q

What are the most common causes of hypoglycaemia?

A

Insulin

Sulphonylureas

Meglitinides

Less common causes: ExPLAIN

Exogenous drugs (as above)
Pituitary insufficiency
Liver failure
Addison’s disease
Islet cell tumours
Non-pancreatic neoplasms

Q

What are the signs of hypoglycaemia?

Adrenergic and neuroglycopenic

A

Adrenergic:
Sweating
Trembling
Hunger

Neuroglycopenic:
Parasthesiae
Blurred vision
Confusion

Hunger is the first sign.

Q

What is Whipple’s triad?

A

A trio of signs that indicate a hypoglycaemic state is pancreatic in origin.

Signs of hypoglycaemia
Plasma glucose is below 3.1mmol/L
Symptoms improve on giving glucose

Q

What is hypoglycaemia?

A

Blood glucose <3.1 mol/L

Q

What are the differentials for hyperosmolar hyperglycaemic state (and DKA)?

A

Lactic acidosis

Starvation ketosis

Alcoholic ketoacidosis

Poisoning

Uraemia acidosis

Q

What are the signs of type 2 diabetes mellitus?

A

May be Asymptomatic

Hyperglycaemia: (primary cause of signs)

Polydipsia
Polyuria
Nocturia
Polyphagia
Fatigue
Weight loss
Blurred vision (hyperglycaemia)

Present as an emergency:

Hyperosmolar hyperglycaemic state
- Hyperventilation, altered mental status, tachycardia, dry mucous membranes, hypotension, N&V

Present with complications:

Neuropathy - diabetic foot ulcer
Retinopathy - visual field loss, 
Nephropathy
Cellulitis
Skin abscess
Cystitis
Pyelonephritis
Vaginal/penile Candida infection
ACS
Stroke
PVD

Q

What are the signs of type one diabetes mellitus?

A

Polydipsia
Polyuria
Nocturia
Fatigue
Weight loss
Blurred vision

Q

What are the pathological processes that occur in the eye to cause diabetic retinopathy?

A

Hyperglycemia causes an over saturation of the sorbitol to fructose pathway, depletes NADH necessary to this step.

Increased sorbitol = (impermeable to membrane) causes osmotic damage to retinal cells.

Formation of advanced glycation endproducts (from reaction of glucose with amino acids) damages blood vessels and nerves.

Capillary leakage > intraretinal haemorrhage > oedema > hard exudates, If in macula > loss of central vision

Capillary occlusion > retinal ischemia > angiogenesis > glaucoma/retinal detachment/vitreous fibrosis

Q

What are differentials for pain in the lower limbs?

A

Peripheral vascular disease - first signs are claudication of the lower limbs

Gout

Osteoarthritis

Q

What is haemachromatosis?

A

A genetic condition caused by mutation of the haemochromatosis gene HFE.
HFE modulates expression of hepcidin (hepatic iron-regulatory hormone).

Low hepcidin expression occurs, which means:

duodenal iron absorption is uninhibited
macrophages continually release iron from erythrophagocytosis (spleen)

This results in elevation in serum iron and transferrin saturation, and deposition of iron in multiple organs; liver, heart, anterior pituitary, pancreas, joints and others.

The iron is an oxidant, which causes fibrosis, and can also cause bronze diabetes (pancreas damage).

Types:
Hereditary - >90% autosomal recessive, white people only
Juvenile - presents in 20/30’s, with cardiomyopathy and hypogonadism
Transferrin receptor 2 - rare
Ferroportin disease -

Q

What are the signs of haemochromatosis?

A

Fatigue

Weakness

Arthralgia

Hepatomegaly

DM

Impotence (Male)

Skin pigmentation

Q

What is ascending cholangitis?

A

This is the acute infection of the common bile duct caused by obstruction, most commonly caused by gall stone, this inflammation ascends towards the liver.

Q

What is primary biliary cholangitis?

A

A chronic autoimmune disease of the small bile ducts within the liver (intrahepatic), causing inflammation and damage.

Q

What is primary sclerosing cholangitis?

A

An autoimmune inflammation of the medium and large biliary ducts, this affects the area in between the intrahepatic ducts (primary biliary cholangitis)and the large biliary ducts (ascending cholangitis).

Q

What is cholecystitis?

A

Inflammation of the gall bladder due to gall stone obstruction of the GB or the GB neck.