GI, kidney Flashcards

1
Q

Functions of the kidney. How much filtrate it clears and urine it makes every day

A

-2 kidneys exchanges water and salts to produce urine which goes into renal pelvis, ureter, bladder, urethra, then outside world.
-180L of filtrate per day
-1.5L urine

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2
Q

Function and structure of a nephron

A

-functional unit of the kidney. Converts blood into urine
1-the glomerulus (filtration occurs)
2. Bowman’s capsule (collects filtrate)
3. Proximal tubule (reabsorption)
4. loop of henle (water and nutrient absorption into blood)
5. distal tubule
6. Collecting duct

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3
Q

How many nephrons in a kidney. Does it increase or decrease with age

A

~1 million
-decreases with age so more likely to have chronic kidney disease

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4
Q

What gland sits on top of the kidney. What hormones it produces

A

Adrenal gland.
cortisol, aldosterone, adrenaline, and noradrenaline

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5
Q

How is kidney function assessed

A

-creatine clearance
-Plasma creatine concentration
-estimated glomerular filtration rate

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6
Q

What is creatine. Normal plasma clearance value in females and male. What high and low values suggests

A

-Creatine is derived from metabolism in skeletal muscles and meat in diet

-95 +/- 20 mL/min in females
-120 +/- 25 mL/min in males

High= low GFR (as glomerulus hasn’t been able to clear filter it)
Low= low muscle mass

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7
Q

What is a healthy GFR. What value do you need dialysis

A

-125 ml/min = healthy
>100 is normal
<10 you need dialysis [stage 5 CKD]

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8
Q

What patients can estimated GMF not be used in

A

Only for people with average heights so Cannot be used in pregnant people, amputees, short people

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9
Q

Explain stage 1-5 of chronic kidney disease: the GFR and treatment

A

1: 90+. Normal function, but urine or structural abnormality.
2: 60-89. Mildly reduced kidney function.
3: 30-59: Moderately reduced renal function.
4: 15-29. Severely reduced Renal function
5. <15. >700 creatine. Endstage kidney failure

Stage 1-3= observe, control BP, address risk factors
Stage 4= Control BP, diet restriction, EPO and vit D supplements. Plan for end stage renal failure.
Stage 5= dialysis, transplant

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10
Q

Risk factors for chronic kidney disease

A

-diabetes
-old age
-polycystic kidneys
-heart disease, Peripheral vascular disease - renal artery stenosis
- ACEI or diuretics, family history of renal problems

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11
Q

Signs and symptoms of CKD (lots.)

A

-hypertension
-normocytic normochromic anaemia -tired, pale, unwell
-anorexic, nausea, vomitting, itch, confusion, agitated
-impaired clotting, increased bleeding
-pulmonary and peripheral oedema, cramps, tremor, twitches
-increased infection risk
-osteodystrophy

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12
Q

What blood components increase and decrease in CKD

A

-Increased BP, creatine, potassium (hyperkalaemia), prostacylin, urea (uraemia)

-low GFR
-reduced EPO (anaemic)
-Low RBC due to marrow fibrosis, renal loss, And increased fragility with consequent early destruction
-reduced vit D and Ca
-reduced vW factor and thromboxane
-impaired platelet adhesion
-metabolic acidosis

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13
Q

How CKD affects drug prescribing

A

-Reduced rate of elimination of renally excreted drugs = may accumulate e.g. opiates
-Reduced protein binding of acidic drugs (eg. phenytoin)
-increased binding of basic drugs (e.g. lignocaine)
-Nephrotoxic drugs may worsen renal function e.g gentamicin, NSAID’s
-immunosupression

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14
Q

Give examples of drugs to avoid and reduce in CKD

A

-Gentamycin (used in prophylaxis) is nephrotoxic = AVOID
-Erythromycin =REDUCE or AVOID if transplant and taking ciclosporin. Makes cyclosporin more toxic
-Dose reduction with acyclovir, amoxicillin, ampicillin, cefalexin, and erythromycin
-Tetracyclines other than doxycycline =AVOID
-NSAIDs =AVOID, except in mild kidney impairment
- BDZ excreted in kidney so IV sedation used in tertiary care

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15
Q

Is prophylaxis required for CKD before dental procedures

A

-Routine prophylaxis is not required for dental procedures, whether they are on dialysis, immunosuppressed transplant patients, have AV fistula

-consider if had infection after previous extraction

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16
Q

Immunosupressants for patients with kidney transplant. Oral side effects

A

-Prednisolone
-Azathioprine
-MMF
-Tacrolimus, sirolimus
-Cyclosporin A

-predisposition to infection - candiosis, herpes. Increased cancer risk (immune system reduced ability to identify abnormal cells). Cyclosporin can cause gingival overgrowth

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17
Q

Although rare, kidney disease is linked with orofacial digital syndrome. What are the signs and symptoms of this

A

-cleft palate
-bifid lobulated tongue
-hypo or hyperdontia
-limb and skeletal abnormalities

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18
Q

What does dialysis involve. Where is a fistula created

A

-remove waste products and excess fluid from the blood when the kidneys stop working properly. It often involves diverting blood to a machine to be cleaned
-patients anticoagulated using heparin (half life 6 hours) to prevent clotting
-arterio-venous fistula at the ACF or wrist (Risk of damage and haemorrhage as very turbulent blood flow)

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19
Q

When is the best time to dentally treat a patient receiving dialysis on heparin

A

-heparin at time of dialysis to prevent clotting in the circuit
-heparin has short half life.
-Day after dialysis = best time to treat these patients as heparin will have worn off but dialysis will have peaked so renal function optimal

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20
Q

What is nephrotic syndrome

A

-Proteinuria with hypoalbuminaemia= too much protein in urine
-Leads to oedema (no oncotic pressure, fluid leaks into tissues)
-Can be secondary to poorly controlled type 2 diabetes

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21
Q

Why osteodystrophy can be a feature in kidney disease

A

-Increased phosphate, decreased plasma Ca
-High PTH which draws calcium out of the bones
-There is a failure in conversion of 25-HCC into 1,25-HCC = leading to secondary hyperparathyroidism

-Also the decreased vit D in CKD causes low plasma Ca

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22
Q

What type of anaemia do CKD patients have

A

normocytic, normochromic anaemia

due to failure production of erythropoietin

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23
Q

Why CKD can impair haemostasis

A

-marrow fibrosis (FULL BLOOD COUNT AFFECTED = reduced platelet count and function so clotting issues)
-Impaired platelet adhesiveness
-Decreased von Willebrand’s factor
-Decreased thromboxane
-Increased Prostacyclin (vasodilation)
-Heparinisation – regular for dialysis

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24
Q

Oral and dental considerations for CKD

A

-Impaired haemsotasis
-Reduced excretion so affects drugs
-Incidence of oral ulceration/ infection increased
-Gingival hyperplasia with ciclosporin
-Beware of skin cancers and increased infection (due to immunosuppression)
-Dialysis patients may experience SIALOSIS
-Palatal and buccal keratosis sometimes seen
-CKD in children= delayed growth, delayed tooth eruption, enamel hypoplasia
-ADVISE PT NOT TO SWALLOW BLOOD POST-EXTRACTION –high protein in blood can exacerbate kidney problems

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25
Q

Causes of acute kidney injury

A

Sudden changes in physiology

-Pre: Vasodilation and Hypotension -Blood or Fluid loss, hypovolemia, sepsis, Dehydration (eg. diarrhoea), Haemorrhage, reduced cardiac output (cardiac arrest) Liver failure. Anaphylaxis
-Kidney stone causing obstruction. Kidney infection
Meds: NSAIDs, ACE inhibitors, gentamicin, metformin, diuretics
-Post: enlarged prostate, UTI, ureter constriction

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26
Q

Signs of acute kidney injury

A

-low urine output or changes to colour
-high creatine (low GFR)
-over time electrolytes change, acidosis, retain fluid (heart failure, kidney failure)
-Not producing enough urine means build-up of potassium which can lead to cardiac arrest if untreated
-nausea and vomiting, confusion, high BP, abdominal pain

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27
Q

Similarities and differences between Ulcerative colitis and Crohn’s

A

-Inflammatory bowel diseases. Genetic and environmental influences. Chronic
-UC= affects large intestine (colon). No oral manifestations (however secondary effects from anaemia)
-Crohn’s= affects anywhere along GI tract from mouth to anus. Oral manifestations

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28
Q

Crohn’s is a transmural process. What is this and consequences

A

-involves the full thickness of the gut wall
-Can develop fistulae. This can become infected and cause an abscess. Can cause obstruction, cause scarring, become necrotic

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29
Q

Signs and symptoms of IBD. systemic signs. Oral features

A

-diarrhoea/ constipation, change in bowel habit, bloating fever, fatigue, abdominal pain/ cramping, mucous or blood in stool, reduced appetite and weight loss.
-recurrent mouth ulcers, gingivitis, diffuse lip swelling, angular cheilitis, cobblestoning of buccal mucosa, glossitis (usually secondary to malabsorption and deficiency of iron, vit B12 or folate)

-Eye problems: episcleritis, uveitis
-Anaemia
-arthirits
-vascular complications
-erythema nodosum
-pyoderma gangrenosum
-malabsorption
-gallstones, kidney stones
-increased risk of cancer

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30
Q

List types of granulomatous diseases

A

Crohn’s disease
TB
Sarcoidosis
Oro-facial granlumatosis

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31
Q

What is proctocolitis and its causes

A

inflammation of the colonic mucosa extending proximally from 15 cm above the anus

-Causes: IBD, sexual intercourse, radiation, ischameia, infection, antibiotic use

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32
Q

What is toxic megacolon and its causes

A

-severe inflammation causes stretching and dilation of colon so muscles stop working causing fluid and gas to build up and toxins can leak into blood stream
-increased risk of c.difficile infection

Causes: IBD, infections, inflammation, bowel ischemia, radiation, and certain medications, antibiotics (clindamycin)

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33
Q

Indications for surgery for IBD

A

-Tx is predominately medical not surgical, as can affect whole chunks of the gut so you don’t want to take out a big chunk to find it recurs somewhere else
-Indications: exsanguinating haemorrhage, failure of medical tx, perforation, suspected cancer

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34
Q

Long term bowel effects of IBD

A

-ulcer perforation, risk of colon cancer, nutritional deficiencies, intestinal strictures, fistulas, anaemia, liver disease
-prednisolone: adrenal crisis, infection, osteoporosis, delayed healing

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35
Q

Causes of dysphagia

A

[difficulty swallowing]
-Cancer
-xerostomia
-neuroogical problems -ability to chew eg. MND
-MYASTHENIA GRAVIS
-Multiple sclerosis – myelin problems causing muscle weakness
-Parkinson’s disease
-Pseudobulbar and bulbar palsy - upper and lower motor neurone palsy of muscles involving swallowing and speech (CN9,10,11,12)
-oesophagitis
-Barett’s oesophagus

36
Q

What is oesophageal varices. Causes

A

-enlarged vessels of the oesophagus which are at risk of rupturing

-Causes by:
Portal Hypertension
Chronic alcohol abuse (dilation)
Liver cirrhosis (blood backs up)
Ingestion of caustic substances (highly acidic)

causes vomitting

37
Q

Oesophagus tests to assess swallowing issues

A

-Oesophagoscopy: camera test with Biopsy
-Barium swallow then x-ray
-CT scan
-Oesophageal Pressure monitoring: Checking if lower oesophageal sphincter opening an closing properly

38
Q

Signs and symptoms to suggest gastric issues. List some types of conditions

A

-Indigestion
-Heartburn, reflux
-Loss of appetite
-Weight loss (H. pylori)
-Vomiting
-Haematemesis (vomiting blood)
-Black stools

Cancer, peptic ulcers, Gastroesophageal Reflux Disease, gastroparesis, gastritis, hiatus hernia

39
Q

Peptic ulcer causes, Symptoms, Consequences

A

-Erosions of stomach or duodenal mucosa caused by gastric acid and pepsin
-Helicobacter pylori
(leads to imbalance with acid secretions on stomach, so more prone to ulcers)
-Prolonged NSAIDs use
-Alcohol, tobacco, stress

-Abdominal pain 1-3 hours after food, feeling full, vomitting, belching, bloating, weight loss, heart burn

-Perforation – leakage into abdomen -> peritonitis
-Haemorrhagic rupture (acute pain, haematemesis, melaena)
-Stricture (narrowing)

40
Q

What not to prescribe patients with peptic ulcers

A

NSAIDs, corticosteroids

41
Q

Function of gastric acid. And Protective mechanisms against gastric acid

A

-HCl activates proteinase pepsin for protein digestion. - inactivates pathogens in food. pH 1.5-2.0.
- secretion by parietal cells.

-Prostoglandins, Mucous (goblet cells) and bicarbonate protects the lining of the stomach

42
Q

Management for peptic ulcers

A

-Stop stress, smoking, alcohol, NSAIDs
-Meds to reduce acid, neutralise acid, protect mucosa
-Triple therapy=H pylori eradication therapy (antibiotics and meds)
-surgery only if haemorrhage, perforation, pyloric stenosis

H2 receptor antagonists
Prostaglandin analogues
Proton pump inhibitors (manipulates the H+ K+ ATPase pump to reduce acid)
Antacids
Chelates and complexes

43
Q

Mechanism of the following medications for peptic ulcers: 1) H2 receptor antagonists. 2) Prostaglandin analogues. 3) Proton pump inhibitors. 4) Antacids. 5) Chelates and complexes

A

1) decreases acid secretion
2) inhibits acid secretion, and stimulate mucous and bicarbonate secretion (PGE=inhibits adenyl cyclase=reduced cAMP)
3) reduces acid secretion (manipulates the H+ K+ ATPase pump)
4) Weak bases that neutralise acid, inactivating pepsin
5) physical barrier coating the mucosa, stimulate bicarbonate and mucous, inhibit action of pepsin

44
Q

Diagnosis and treatment for H.Pylori infection

A

(can lead to stomach ulcers)
-Diagnosis: urea breath test, stool antigen test, endoscopy/ gastroscopy
-Treatment= triple therapy for 1 week:
1. PROTON-PUMP INHIBITOR
2CLARITHROMYCIN
3METRONIDAZOLE OR AMOXICILLIN
-Managed with lifestyle factors, cessation of NSAIDs, smoking, alcohol

45
Q

What type of anaemia is gastric problems associated with

A

Pernicious anaemia = deficiency of intrinsic factor (AUTOIMMINE) – B12 DEFICIENCY ANAEMIA (macrocytic RBCs)

46
Q

Symptoms of Barett’s oesophagus

A

=Metaplasia. Oesophagus epithelial cells undergo change. Can be caused by acid reflux

Heartburn.
Indigestion.
Blood in vomit or stool.
Dysphagia
Nocturnal regurgitation (acidic or bitter liquid coming up to the chest or mouth during the night)

Increased risk of cancer

47
Q

What is GORD. Risk factors and symptoms. Management

A

-Retrograde flow of gastric contents into oesophagus
-Only present when reflux of gastric contents causes frequent, severe symptoms or mucosal oesophagus damage from the HCl acid (eg. barett’s oesophagus)
-due to low pressure of lower oesophageal sphincter
-heartburn, regurgitation of acid or bile, retrosternal discomfort, excess salivation, pain on swallowing dental erosion, hoarseness
-Risk factors: age, stress, obesity, large meals especially at night, alcohol, caffeine, pregnancy, hiatus hernia
-Tx: lose weight, Proton pump inhibitor (omeprazole/ lansoprazol) Antacids (Gaviscon)

48
Q

Types of stomach tests

A

-Gastroscopy: Offers direct vision and Biopsy information
-Histology and tests for Helicobacter pylori
-CT Scan
-Barium Meal and Tests of gastric function (now used less)

49
Q

duodenum, Jejenum and ileum tests

A

[all are components of the small intestine]

-Duodenum: Gastro-Duodenoscopy for direct vision and Biopsy. Not long enough to go beyond duodenum. CT scan

-Jejenum and ileum: direct vision not possible. CT scan. Barum follow-through

50
Q

Does coeliac disease primarily affect small or large bowel. What genes are involved

A

small
-a-gliadin in gluten isn’t usually recognised, but its modification in the disease causes an inflammatory reaction to it causing gut damage
-an immune reaction to eating gluten.
variants of the HLA-DQ2 and HLA-DQ8 genes

51
Q

What is diverticolitis and does it affect large or small bowel. Where is the pain usually. Complications

A

-large bowel
-small pouches form in the colon wall and can become infected
-colicky pain, fever and abnormal bowel habits
-Pain in lower left quadrant
-common in 65+.
-complications= perforation, peritonitis, abscess, fistula, bleeding, stricture

52
Q

Types of colon and rectum tests

A

-Colonoscopy/Flexible sigmoidoscopy:direct vision, Biopsy
-Barium enema
-Special tests to determine transit times

53
Q

Anorectal conditions: types, symptoms, tests

A

-Bleeding – haemorrhoids
-Pain
-Tenesmus – feeling of incomplete evacuation of bowel contents
-Prolapse
-Incontinence

IDB
Carcinoma of rectum (weight loss, change in bowel habits, growths around rectum)
Haemorrhoids
Fissure – tear in skin around rectum
Fistula
proctocolitis

-Direct vision: Proctoscopy / Rigid/ flexible sigmoidoscopy
-Digital examination
-Pelvic CT
-Trans Rectal Ultrasound

54
Q

Common causes of blood in stools

A

Haemorrhoids
Anal Fissure
Diverticular disease
Cancer
IBD
Infective Colitis
Vascular malformations

55
Q

What conditions have high ACE serum level

A

-sarcoidosis
-TB
-Primary biliary cirrhosis
-Addison’s

a biomarker to reflect the damage of endothelial cells

56
Q

Causes of recurrent oral ulceration

A

[discludes traumatic ulcers]
-Crohn’s disease
-iron, folate, vit B12 deficiency
-coeliac disease
-drugs (NSAIDs, B blockers, Nicorandil)
-allergy
-hormones
-Behcet’s syndrome
-Reiter’s syndrome
-Cyclic neutropenia
-PFAPA syndrome

57
Q

Bile function, production, storage

A

Bile made in the liver, stored in the gall bladder. Bile needed for absorption of fat
-RBCs broken down into bilirubin. Liver cells process bilirubin into bile.

58
Q

Causes of bilary obstruction

A

-stone disease= gall stones that form within the liver and then get lodged in the bile ducts
-strictures (narrowing)= benign or malignant cancer, inflammation

59
Q

Signs and symptoms of biliary disease (bile duct and gallbladder)

A

-Pain: Epigastric or UR quadrant of abdomen. May radiate into the back. Acute or chronic. Exacerbated by movement
-Jaundice
-Nausea +/- vomiting
-Fever
-Weight loss
-Bloating, pale greasy stool (Pancreatic exocrine insufficiency)
-Poor diabetic control / new onset diabetes
-Or no symptoms at all!

60
Q

Signs and symptoms of jaundice. The Causes of obstructive and non-obstructive

A

=High bilirubin
-Yellow skin and sclera of eyes. Itchy skin. Red palms. Spontaneous bleeding. Dark urine, pale stool (bile no longer entering GI tract, goes into urinary tract)

1-obstructive jaundice: biliary obstruction from gallstones or biliary strictures

2-Non-obstructive jaundice:
-primary liver disease (cirrhosis), hepatitis = Liver cells cannot process bilirubin into bile.
-Haematological problems = excessive breakdown of RBCs into bilirubin

61
Q

Prehepatic, hepatocellular and post-hepatic causes of jaundice/liver disease

A
  1. Increased breakdown of RBC into bilirubin -sickle cell anaemia, thalassemia. Or defect in bilirubin metabolism (Gilbert’s)
  2. Liver Inability to metabolise and excrete bilirubin- hepatitis, cirrhosis, alcohol, paracetamol overdose, thrombos, congenital disorders
  3. Aka obstructive. Blocked hepatic duct, Gallstones, pancreatic cancer, strictures
62
Q

What increases someones risk getting jaundice

A

drug and alcohol abuse
bleeding problems
blood transfusion
hep infection

63
Q

How liver function test differs in obstructive and non-obstructive jaundice. What will be elevated in alcohol associated jaundice

A

-very high ALT and AST in non-obstructive (as this is caused by liver disease, unlike obstructive)
-gamma glutamyl transpeptidase raised in alcoholics (and AST>ALT)
-increased bilirubin in all types

64
Q

For obstructive jaundice, what causes painful and painless symptoms

A

-Painful=stones in bile duct
-Painless=more worrying. Biliary strictures due to inflammation or malignancy

65
Q

What clotting factors are made and stored in the liver

A

2,7,9,10

66
Q

Complications that can arise due to obstructive jaundice. Treatment

A

1-Infection of bile duct (ascending cholangitis) = fever, abdominal pain, jaundice
-Antibiotics, biliary decompression
2-Abnormal coagulation: prolonged prothrombin time=increased bleeding
-IV vit K

67
Q

Presentation of gallstones. Complications that can arise

A

-Usually asymptomatic
-can be painful after eating if sits in cystic duct or common bile duct

-obstructive jaundice
-infection
-ischaemic gallbladder
-prolonged prothrombin time=increased bleeding
-acute pancreatitis

68
Q

Presentation and causes of acute pancreatitis

A

-due to gallstones, alcohol, drugs, hyperlipidemia, trauma, high blood calcium, idiopathic
-Severe upper right abdominal pain into back, multi-organ failure, pancreatic necrosis, pseudocysts, vomitting

69
Q

Presentation and causes of chronic pancreatitis

A

-Chronic inflammatory process causing gland fibrosis, loss of parenchymal function and strictures in the pancreatic duct
-Due to alcohol, genetics, recurrent acute inflammation, cystic fibrosis,

-Pain
-Exocrine insufficiency (eg. pale greasy stool)
-Endocrine insufficiency
-Jaundice

70
Q

Management of 1) acute and 2) chronic pancreatitis

A

1) manage underlying cause
2) manage underlying cause, pain management, stop smoking and drinking, surgery, pancreatic enzyme replacement

71
Q

Likely cause if pain is in upper right abdomen and radiates to the back

A

biliary disease, acute pancreatitis

72
Q

Causes of colicky abdominal pain

A

-comes in waves, due to obstruction of a hollow organ

Bowel colic (IBD)
Renal colic (kidney or urinary stones)
Biliary colic (gallstones)
Uterus/ fallopian tubes
Appendix

73
Q

Signs and symptoms of peritonitis

A

-Localised sharp Pain felt in area of inflammation
-Worse with movement, coughing, inspiration
-Rigid when palpating, Rebound tenderness/ percussion tenderness
-Absent bowel sounds

74
Q

Causes, Signs and symptoms of appendicitis

A

-Caused by obstruction of appendix lumen (calcified faeces, infection, inflamed lymph tissue, cancer)

-Initial central, generalised, colicky pain
-Becomes localised to Lower right when affects peritoneum
-Usually other lower GI symptoms (change in bowel habits etc.)
-Usually mild temperature and WBC rise and inflammatory markers

75
Q

Mesenteric adenines causes and symptoms

A

-Enlarged mesenteric lymph nodes
-Usually in children and adolescents

Associated with URTI, earache, sore throat, headache, photophobia
-High temp
-Tenderness and pain not focal
-WCC raised – lymphocytes

76
Q

4 cardinal features of intestinal obstruction

A

pain, bloating, vomiting, absolute constipation

due to herniation, scarring, tumour

77
Q

What abdominal disease will have raised amylase

A

Pancreatitis

78
Q

What are the pain symptoms of these gallbladder diseases: biliary colic (gallbladder stone), cholecystitis (inflamed gallbladder), cholangitis (infection due to gallstone)

A

1) Biliary colic –short attacks (4 hours) - comes in waves
2)Cholecystitis –longer attacks + evidence of inflammation – temperature, raised WBC
3) Cholangitis –Charcot’s triad: Pain, fever, jaundice

79
Q

What is Charcot’s triad

A

3 signs of cholangitis (infection due to gallstone in common bile duct or cystic duct)
=fever, abdominal pain, jaundice

80
Q

Difference between upper and lower GI organs and symptoms

A

1) upper GI= esophagus, stomach, duodenum
-heartburn, dysphagia, reflux, vomitting, abdominal pain

2) lower = anus, rectum, small and large intestines, cecum
-changed bowel habits, blood in stools, abdominal pain

81
Q

Meds that are bad for the kidneys

A

NSAIDs
ACE inhibators
Diuretics
Gentamicin
Metformin

82
Q

What deficiency do alcoholics have

A

B12

83
Q

Specific questions in a history for GI disorders

A

Diet/appetite
Weight loss – over what period
Dysphagia (swallowing difficulty)
Bowel habit (change)
Medications – either those which may precipitate abdominal pain or those which may be used to treat it
Nausea/vomiting
Smoking/alcohol intake

84
Q

Questions in a history for someone with jaundice

A

Drug/alcohol history
Bleeding problems
History of blood transfusion
History of drug abuse
History of foreign travel
History of sexual promiscuity
Pale stool/dark urine (suggests obstructive jaundice)
Ask about previous immunisation against infective hepatitis
Find out details of the patient’s occupation

85
Q

Signs and symptoms of liver disease

A

-spider nevi
-increased PT
-Petichiae purpura
-Portal venous hypertension - vomitting blood, ascites
-jaundice
-dupuytrens
-streatorhorrea - pale poo as no bilirubin getting into GI tract to darken it
-sialosis - swelling of salivary glands
-flapping tremor
-encephalitis (build up of toxins)
-Palma erythema