Review of posters 04/05/2016 Flashcards

1
Q

Diverticulosis

A

Presence of diverticula

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2
Q

Diverticulitis

A

Inflammation and infection of the diverticula.

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3
Q

Pathophysiology of diverticulitis

A

Outcropping (diverticula) has a neck. This can become blocked by faeces-which means the faeces there is stagnent. This allows bacteria time to infect the diverticula causing diverticulitis.

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4
Q

Symptoms of diverticulitis

A
Fever
Severe LIF pain 
Constipation
Tachycardia
Febrile
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5
Q

Where does diverticulitis normally occur?

A

Sigmoid colon

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6
Q

On examination of diverticulitis, what would you observe/

A

Tenderness, rigidity and gaurding

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7
Q

Treatment of mild diverticulitis.

A

Antibiotics- ciproflaxacin and metronidazole.

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8
Q

Treatment of severe diverticulitis

A

Hospital admission, fluids, antibiotics.

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9
Q

Do people with diverticular disease but without acute diverticulitis have symptoms?

A

nope

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10
Q

What dietary advice would you give someone with diverticular disease?

A

Increase dietary fibre.

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11
Q

If someone is symptomatic however does not have acute diverticulitis- what investigations would you perform?

A

Colonoscopy, barium enema, flexible sigmoidoscopy

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12
Q

What would investigations into acute diverticulitis show?

A

raised CRP and ESR

Ultrasound and colonscopy showing thickening of the colonic wall.

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13
Q

What is non-alcoholic fatty liver disease?

A

Presence of fat deposits in the liver.

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14
Q

How does NAFLD occur?

A

Intake of too much fat in diet. (same consequences would be seen with alcohol however would not be called NAFLD)

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15
Q

What is non-alcoholic steatohepatitis?

A

Development of NAFLD (condition worsened)

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16
Q

How is fat content in a healthy liver balanced?

A

By oxidation of triglycerides and fatty acid export keeping the fat content low. And lipogenesis and uptake of free fatty acids offering a balance by taking in fat to the liver.

17
Q

Pathophysiology of NAFLD.

A

Lipoproteins circulate in the blood- these are made up of triglycerides. Hormone induced lipase breaks this down into free fatty acids which are taken up by the liver hepatocytes. The free fatty acids in the liver hepatocyte can either go on to re-form the triglycerides (bad) or go through oxidation (good).
PPAR alpha- comes into play when there is excess energy. If it is effective- it will increase oxidation of free fatty acids, however if it is defective it will increase storage as triglycerides. This allows fat to build up in the liver.

18
Q

How does NAFLD develop onto NASH

A

Inflammation occurs. Fat accumalation, liver cell necrosis and fibrosis.

19
Q

When does NAFLD progress to become irreverisble?

A

Both NASH and NAFLD are reversible. However if NASH was to develop further to cirrhosis- this would not be reversible

20
Q

What is the treatment of NAFLD and NASH?

A

WEIGHT LOSS AND EXERCISE.

21
Q

How would you investigate NAFLD or NASH?

A

Ultraosund

liver biopsy

22
Q

Ventricular septal defect

A

This is a common congenital defect where there is a hole between the ventricles allowing blood to flow through.

23
Q

Describe the consequences of ventricular septal defect

A

Left to right shunt occurs. Due to blood being under more pressure in the left side of the heart than the right- blood will move from a higher pressure to a lower pressure.
This will increase the amount of blood in the right side of the circulation and can cause pulmonary hypertension.

24
Q

Describe the two types of ventricular septal defect.

A

Small VSD- may be asymptomatic- no abnormal ECG or CXR findings.
Large VSD- significant left to right shunt. Pulmonary arteries may be more prominent on CXR due to increased flow. Also shows cardiomegaly.
Echo- will assess hole size and haemodynamic consequence.

25
Q

Treatment of VSD

A

Surgical intervention- this should happen when the atria start to become affected.

26
Q

Atrial septal defect

A

Hole between the atria

27
Q

Where can ASD occur?

A

Sinus venosus- by the SVC or IVC
Ostrium secundum- mid septum
Ostrium primun- lower part of septum

28
Q

What happens in ASD

A

Significant left to right shunt results in right heart overload and dilatation.

29
Q

Symptoms of ASD

A

Breathlessness, exercise intolerance, atrial arrhythmias

Right ventricular heave

30
Q

Investigations and treatment of ASD

A

Prominent pulmonary arteries on CXR

Right bundle branch block and right axis deviation on ECG

31
Q

Patent ductus arteriosus

A

Ductus arteriosus (connection between the proximal left pulmonary artery and the descending aorta) fails to close

32
Q

What symptoms/signs would you see from patent ductus arteriosus?

A

Machine like murmur

33
Q

treatment of patent ductus arteriosus?

A

Indometacin (prostaglandin inhibitor)

34
Q

Co-arctation of the aorta

A

Narrowing of the aorta at the ductus arteriosus

35
Q

Symptoms of co-arctation of the aorta

A

Often asymptomatic
Hypertension in upper limbs
Weak, delayed pulses in lower limbs

36
Q

Treatment of co-arctation fo the aorta

A

Baloon dilatation
stenting in older children
Surgical repair in neonates.

37
Q

Cyanotic heart disease

A

Fallots tetralogy

38
Q

What is fallots tetralogy

A
A large malaligned ventricular septal defect
An overiding (aorta is directly over the ventricular septal defect) aorta
Right ventricular outflow obstruction
Right ventricular hypertrophy
39
Q

Treatment of cyanotic heart disease

A
Pulmonary shunts
Postural manoeuvres (squatting)