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PANREAS 1__ صالح Flashcards

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1
Q

what’re the boundries of the pancreas ?

A

the tail of the pancreas is close to the spleen and the head near to the dudenum .

the tail of the pancreas is very vascular so any injury lead to heamoltical instability .

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2
Q

what the composition of the pancreas ?

A

-The main pancreatic duct branches into interlobular and intralobular ducts, ductules and, finally, acini.

80–90% is composed of exocrine acinar tissue, which is organized into lobules

Clusters of endocrine cells, known as islets of Langerhans, are distributed throughout the pancreas. Islets consist of different cell types: 75 per cent are B cells (producing insulin); 20 per cent are A cells (producing glucagon); and the remainder are D cells (producing somatostatin) and a small number of pancreatic polypeptide cells.

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3
Q

The main duct is lined by

A

The main duct is lined by columnar epithelium, which becomes cuboidal in the ductules. Acinar cells are clumped around a central lumen, which communicates with the duct system.

تتجمع حول تجويف مركزي

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4
Q

what the role of pancreas during the meal?

A

In response to a meal, the pancreas secretes digestive enzymes in an alkaline (pH 8.4) bicarbonate-rich fluid

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5
Q

what’re the stimulation to release the pancreatic enzyme ?

A
  • INTESTINAL PHASE

Secretin acts in tandem (بالتزامن)with another hormone called cholecystokinin (CCK)that produce by the deudenum Not only does CCK stimulate the pancreas to produce the requisite pancreatic juices, it also stimulates the gallbladder to release bile into the duodenum.

(so the lipid in protein stimulate the secretion )

-CEPHALIC PHASE

Vagal stimulation increases the volume of secretion. During this phase, the proteolytic enzymes ( e.g amylase, lipase, trypsin, elastase and chymotrypsin ) are in an inactive form, the maintenance of which is important in preventing pancreatitis.

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6
Q

what’s the general investigation of the pancreas ?

A

-Serum levels of proteolytic enzymes

like amylase, lipase, trypsin, elastase and chymotrypsin
directly measuring pancreatic secretion in response to a standardized stimulus.
e.g. ingestion of a test meal, as in the Lundh test, or pharmacological, e.g. intravenous injection of a hormone, such as secretin or CCK

-Imaging
Ultrasound.
C.T scan. ( Computerized tomography)
MRI ( MRCP) ( magnetic resonance cholangiopancreatography)
ERCP. ( endoscopic retrograde cholangiopancreatography)
Endoscopic ultrasound

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7
Q

Cystic fibrosis

A

is congintal abnormality of the pancreas

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8
Q

Pancreas divisum

A

Congenital diseases

embryological ventral and dorsal parts of the pancreas fail to fuse. Usually asymptomatic but have a higher incidence of acute , chronic pancreatitis and pancreatic pain

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9
Q

how to diagnosis the pancreas divisum ?

A

diagnosis can be arrived at by MRCP, EUS or ERCP, augmented by injection of secretin if necessary

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10
Q

what ‘s the treatment of the pancreas divisum ?

A

-Endoscopic sphincterotomy + stenting of the minor papilla

  • sphincteroplasty,
  • pancreatojejunostomy or even resection of the pancreatic head

+sphincterotomy is a simple surgery during which the sphincter is cut or stretched

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11
Q

Annular pancreas

A

failure of complete rotation of the ventral pancreatic bud during development, so that a ring of pancreatic tissue surrounds the second or third part of the duodenum

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12
Q

when we see the annular pancreas ?

A

seen in association with congenital duodenal stenosis or atresia and is therefore more prevalent in children with Down’s syndrome.

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13
Q

presentation of the annular pancreas ?

A

. Duodenal obstruction typically causes vomiting in the neonate .

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14
Q

treatment of the annular pancreas ?

A

duodenoduodenostomy

anastomosis for the purpose of bypassing an obstructed segment of duodenum.

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15
Q

why the blunt trauma is infrequent in pancreas ?

A

because of the pancreas location retroperitoneally sourround by the viscera

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16
Q

what the source of the blunt of the pancreas ?

A

it is often concomitant with injuries to other viscera, especially the liver, the spleen and the duodenum.

Occasionally, a forceful blow to the epigastrium may crush the body of the pancreas against the vertebral column.
ضربة قوية

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17
Q

how the pt with blunt presented with ?

A
  • usually presents with epigastric pain minor at first then develop more severe pain due to the sequelae of leakage of pancreatic fluid into the surrounding tissues.
  • A rise in serum amylase occurs in most cases.
  • A CT scan of the pancreas will delineate the damage
  • ERCP and MRCP If there is doubt about duct disruption,
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18
Q

Treatment of blunt injuries

A
  • we should first make sure whether the pancreatic duct has been disrupted
  • intravenous fluids and a nil by mouth regimen while these investigations are performed
  • no need to rush to a laparotomy if the patient is haemodynamically stable, without peritonitis
  • preferable to manage conservatively at first, investigate
  • Operation is indicated if there is disruption of the main pancreatic duct; in almost all other cases, the patient will recover with conservative management.
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19
Q

Penetrating injury

A
  • Need urgent surgery. by Haemostasis and closed drainage for minor parenchymal injuries
  • distal pancreatectomy should be performed, with or without splenectomy if the gland is transected in the body or tail
  • but if the plane of transection is flat and clean anastomose the stump of the distal pancreas to a Roux loop of jejenum as an end-to-side pancreatojejunostomy.
  • if there is severe injury to the pancreatic head and duodenum, then a pancreatoduodenectomy may be necessary
  • If damage is purely in the head of the pancreas, haemostasis and external drainage is normally effective.
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20
Q

Iatrogenic injury ( VERY IMPORTANT)

A

its damage happen due to some medical surgery

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21
Q

what’re the causes of the Iatrogenic injury ?

A

-splenectomy
may cause tail injury resulting in a pancreatic fistula.

  • Billroth II gastrectomy
    cause Injury to the accessory pancreatic duct (Santorini), which is the main duct in 7 per cent of patients,

-Enucleation of islet cell tumors of the pancreas
can result in fistulae

استئصال

-sphincterotomy
cause Duodenal or ampullary bleeding this need duodenotomy to control the bleeding.

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22
Q

Pancreatic fistula (IMPORTANT) cause

A
  • Trauma

- Acute and chronic pancreatitis

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23
Q

Site of Pancreatic fistula

A

externally to skin or internally to bowel

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24
Q

the diagnosis of Pancreatic fistula

A

measurement of the amylase in the fistula content

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25
the treatment of Pancreatic fistula
- correction of metabolic and electrolyte disturbances IVF - parenteral or nasojejunal nutritional support - drainage of the fistula into a stoma bag with protection of the skin - When there is obstruction within the pancreatic duct, stenting the duct endoscopically - use of octreotide will also suppress pancreatic secretion +octreotide mimics natural somatostatin pharmacologically, though it is a more potent inhibitor of growth hormone, glucagon, and insulin than the natural hormone.
26
The pancreas is situated
in the retroperitoneum.
27
pancreas divided into
- into a head, which occupies 30% of the gland by mass, | - a body and tail, which together constitute 70 %
28
The head of pancreas lies
within the curve of the duodenum, overlying the body of the second lumbar vertebra and the vena cava.
29
behind the neck of the pancreas
-The aorta and the superior mesenteric vessels -Behind the neck of the pancreas, near its upper border, the superior mesenteric vein joins the splenic vein to form the portal vein
30
Coming off the side of the pancreatic head pass to Lt
Coming off the side of the pancreatic head and passing to the left and behind the superior mesenteric vein is the uncinate process of the pancreas
31
The tip of the pancreatic tail
extends up to the splenic hilum.
32
Weight of pancreas
Weight = 80 grams
33
Acute pancreatitis
acute condition presenting with - abdominal pain and usually associated with - raised pancreatic enzyme levels in the blood or urine as a result of pancreatic inflammation
34
Acute pancreatitis cause
premature activation of pancreatic enzymes within the pancreas, leading to a process of autodigestion.
35
the sequele of the Acute pancritis ?
_Anything that injures the acinar cell and impairs the secretion of zymogen granules or damages the duct epithelium and thus delays enzymatic _premature activation of pancreatic enzymes _cellular injury has been initiated _the inflammatory process can lead to pancreatic oedema haemorrhage and, eventually, necrosis _inflammatory mediators are released into the circulation, systemic complications such as -haemodynamic instability -bacteraemia (due to translocation of gut flora) - acute respiratory distress syndrome - pleural effusions - gastrointestinal haemorrhage renal failure -disseminated intravascular coagulation (DIC) +Zymogen granules (ZGs) are specialized storage organelles in the exocrine pancreas that allow the sorting, packaging and regulated apical secretion of digestive enzymes. ZG constituents play important roles in pancreatic injury and disease. The molecular mechanisms underlying these processes are still poorly defined.
36
classification of acute panceritis
``` Mild is characterised by -interstitial oedema of the gland -minimal organ dysfunction 80% - Mortality 1% ``` ``` Severe acute pancreatitis is characterised by -pancreatic necrosis, a severe systemic inflammatory response -often multi-organ failure. - mortality varies from 20 to 50 % ``` About one-third of deaths occur in the early phase of the attack, from multiple organ failure death after the first week of onset are due to septic complications
37
what're the causes of the death in acute pancritis ?
1/3 of death in the early phase of the attack, from multiple organ failure death after the first week of onset are due to septic complications
38
causes of acute pancritis ?
-Idiopathic - Gallstones - Ethanol - Trauma,Tumer of ampulary of vater - Steroids - Mumps, malnutrient - Autoimmune - Scorpian venom - Hyperlipidaemia, hypothermia, hypercalcaemia, hyperthyrodism - ERCP - Drugs I GET SMASHED and all the congintal pancreas disease
39
Clinical presentation of acute pancritis
history --------------- -Pain is dull ,sever, develops quickly, reaching maximum intensity within minutes and persists for hours or even days ,constant and refractory to the usual doses of analgesics Pain is usually experienced first in the epigastrium but may be localized to either upper quadrant or felt diffusely throughout the abdomen There is radiation to the back in about 50 per cent of patients, some patients may gain relief by sitting or leaning forwards - Nausea, repeated vomiting and retching - Why ? Hiccough ``` general exam ----------------------- -the appearance -Tachypnea -tachycardia - hypovolemia and neurogenic shock -The body temperature raised because its systemic ``` -Mild icterus (technical term for jaundice) can be caused by biliary obstruction in gallstone pancreatitis - (Grey Turner’s sign) - (Cullen’s sign) - Subcutaneous fat necrosis may produce small, red, tender nodules on the skin of the legs. Abdominal examination ------------------------------------ - distension due to ileus happen due to paralysis - mass can develop in the epigastrium due to inflammation - usually muscle guarding in the upper abdomen, although marked rigidity is unusual - A pleural effusion is present in 10–20 per cent of patients - Pulmonary oedema and pneumonitis - confused encephalopathy - the signs of metabolic derangement together with hypoxaemia
40
acute pancreatitis can mimic
most causes of the acute abdomen
41
acute swinging pyrexia with pancritits suggests
suggests cholangitis
42
Mild icterus with pancritits
caused by biliary obstruction in gallstone pancreatitis
43
What are signs of acute pancreatitis?
``` Tachycardia Pyrexia Can be in profound shock Jaundice - obstructive Ileus Rigid abdomen +/- local/general tenderness Cullen's sign Turner's sign ```
44
What is characteristic of the pain experienced in acute pancreatitis?
Radiates to the back | Relieved by sitting forward
45
What is Cullen's sign?
Periumbilical ecchymoses
46
What is Grey Turner's sign?
Ecchymoses or purple discolouration of the flanks.
47
Differential of the acute pancritis ?
- Biliary disease - Intestinal obstruction - Mesenteric Ischemia - MI (inferior) - AAA ( abdominal aortic aneurism) - Distal aortic dissection - PUD similar in pain ++ Pulmonary oedema and pneumonitis are also described and may give rise to the differential diagnosis of pneumonia or myocardial infarction.
48
Evaluation of pt acute pancritis ?
+Bloods - Amylase/lipase inflammatory markers others +Abdominal XR/Erect CXR +Abdominal USS +Contrast-enhanced spiral CT +MRI/MRCP +ERCP
49
why we perform Amylase/lipase ?
+amylase…Nonspecific !!! ------------------------------------------- so if Amylase levels > 3x normal very suggestive of pancreatitis but May be normal in chronic pancreatitis!!! Enzyme level  severity False (-): acute on chronic alcoholism ; HyperTG False (+): renal failure, other abdominal or salivary gland process, acidemia lipase ---------------- More sensitive & specific than amylas
50
when the level of amylase give false results ?
False (-): acute on chronic alcoholism ; HyperTG means he have the pancritis but the result is low or normal False (+): - renal failure, - abdominal or salivary gland process may be because eating ? -acidemia
51
does normal amylase level exclude pancritis ?
no its may be false (-)in choronic alchohlic | oe normal in chronic pancrititis
52
why we measure the inflammtory marker ?
- elevated CRP, IL-6, IL-8 (studies hoping to use these markers to aid in detecting severity of disease) -ALT > 3x norma in gallstone pancreatitis (96% specific, but only 48% sensitive) rememmber may pt have jauindice
53
what wee see in blood test beside the amylase and the inflammatory marker ?
-decrease Ca and glucose ( Fatty acids produced by lipolytic enzyme breakdown of fat bind calcium, forming white deposits decrese the cc and may be renal glucose because of the decrese the insulin ) - increase in WBC ,Heamtocrite , Urea
54
why we perform the AXR ?
to see small bowel ileus (lack of movement in the intestines.) from food stasis
55
why we perform the us or ct ?
may show enlarged pancreas with - abscess, - fluid collections, - hemorrhage, - necrosis - pseudocyst
56
why we perform ERCP ?
to see the dilation in the pancritic duct if there is dilation
57
Morbidity and mortality highest if
necrosis present (especially if necroctic area infected)
58
Dual phase CT scan useful for
initial reveal for necrosis
59
how to estimate the prognosis of the AP ?
- Ranson (most popular ) - APACHE II - CT severity Index - Imrie Score.
60
what's the most predective prognotic criteria for the AP?
CT severity Index this to be most predictive of adverse outcomes if CT score > 5 associated with 15x mortality rate
61
proplem in CT severity Index is
1 CT study showing this was conducted 72 hours after admission (Ranson/Apache are 24 & 48 hours) 1 دراسة CT تظهر أن هذا تم إجراؤه بعد 72 ساعة من القبول (Ranson / Apache هي 24 و 48 ساعة)
62
Ranson Criteria
``` Admission Age > 55 WBC > 16,000 Glucose > 200 LDH > 350 AST > 250 ``` ``` During first 48 hours Hematocrit drop > 10% Serum calcium < 8 Base deficit > 4.0 Increase in BUN > 5 Fluid sequestration > 6L Arterial PO2 < 60 ```
63
Age for RC
> 55
64
WBC
> 16,000
65
Glucose
> 200
66
LDH
> 350
67
AST
250
68
Hematocrit
> 10%
69
Serum calcium
< 8
70
Base deficit
> 4.0
71
BUN
> 5
72
Fluid sequestration
> 6L
73
Arterial PO2
< 60
74
Ranson Criteria if 2 signs
5% mortality risk with <2 signs 15-20% mortality risk with 3-4 signs 40% mortality risk with 5-6 signs 99% mortality risk with >7 signs
75
Ranson Criteria if 2 signs
5% mortality risk
76
Ranson Criteria if 3-4 signs
15-20%
77
Ranson Criteria if 5-6 signs
40%
78
Ranson Criteria if >7 signs
99%
79
In the glasgow criteria for severity of pancreatitis, what threshold is used for WBC?
> 16,000
80
In the glasgow criteria for severity of pancreatitis, what threshold is used for age?
> 55
81
In the glasgow criteria for severity of pancreatitis, what threshold is used for glucose ?
> 10ml/l but no history of DM
82
In the glasgow criteria for severity of pancreatitis, what threshold is used for urea ?
> 16 mmol/l
83
In the glasgow criteria for severity of pancreatitis, what threshold is used for po2?
< 60
84
In the glasgow criteria for severity of pancreatitis, what threshold is used for ca ?
< 2 mmol/l
85
In the glasgow criteria for severity of pancreatitis, what threshold is used for alb ?
< 32 mmol/l
86
In the glasgow criteria for severity of pancreatitis, what threshold is used for LDH ?
> 600
87
In the glasgow criteria for severity of pancreatitis, what threshold is used for ALT /AST ?
> 600
88
CT grade
CT Grade A is normal (0 points) B is edematous pancreas (1 point) C is B plus extrapancreatic changes (2 points) D is severe extrapancreatic changes plus one fluid collection (3 points) E is multiple or extensive fluid collections (4 points)
89
what're the parameters of the ct ?
Necrosis score None ________(0 points) < 1/3________ (2 points) (1/3 - 1/2)_____(4 points) > 1/2 ________(6 points) TOTAL SCORE = CT grade + Necrosis
90
Therapy of AP
-Remove offending agent (if possible) as if there is stone removed by ERCP and biliary sphincterotomy within 72 hours - Supportive !!! * NPO with NG suction for patients with ileus or emesis * Aggressive volume repletion with IVF cuze the pancrease sequestre all the fluid - 3- Narcotic analgesics 4- Don’t forget PPI to prevent stress ulcer
91
Necrotizing pancreatitis found by
on CT with IV contrast
92
what's the complication of AP ?
-Necrotizing pancreatitis -Pseudocysts this Cyst may become infected, rupture, hemorrhage or obstruct adjacent structures may be Asymptomatic, non-enlarging pseudocysts so do imaging but if it Symptomatic, rapidly enlarging or complicated pseudocysts need to be decompressed -Fistula formation -Infection abscess, pancreatic necrosis, infected pseudocyst, cholangitis, and aspiration pneumonia -> SEPSIS may occur -Renal failure Severe intravascular volume depletion or acute tubular necrosis may lead to ARF -Pulmonary Atelectasis, pleural effusion, pneumonia and ARDS can develop in severe cases -Metabolic disturbances hypocalcemia, hypomagnesemia, hyperglycemia -GI bleeds Stress gastritis
93
Pseudocysts charatrize by
- persistent pain | - continued high amylase levels (may be present for 4-6 wks
94
how to investigat infection in the AP ?
If concerned, obtain cultures and start broad-spectrum antimicrobials (appropriate for bowel flora) otherwise In the absence of fever or other clinical evidence for infection, prophylactic antibiotics is not indicated
95
how to prevent GIT complication ?
by PPI
96
what the prognosis of pt with AP after therby ?
+ mild, self-limited Usually resolves in 3-7 days +severe requiring ICU admission Mortality may approach 50% in severe cases
97
which most common sever or mild cases of IP ?
mild is 85%-90% sever 15%-10%
98
Chronic pancreatitis pathophysiology ?
- irreversible parenchymal destruction leading to pancreatic dysfunction andloss of exocrine acinar cells and a marked increase in interstitial fibrous connective tissue. - The islets of Langerhans are preserved and constitute a relatively greater proportion of the pancreatic tissue - may be Hyperplasia of islet cells is also seen - sizes and number of nerves are increased - protective perineural sheath is damaged - damage for the nerves are found in proximity to inflammatory foci - appear to be selective increases in certain peptidergic nerves * peptidergic nerves are intrinsic to the gut,
99
cause of pain in chronic pancreatitis
- sizes and number of nerves are increased - damage for the nerves are found in proximity to inflammatory foci - protective perineural sheath is damaged --appear to be selective increases in certain peptidergic nerves
100
Chronic pancreatitis eitology?
#1- etiology is chronic EtOH abuse (90%) ``` Gallstones Hyperparathyroidism Congenital malformation (pancreas divisum) Idiopathic ``` MRCP of pancreas divisum I get smashed
101
Presentations of cp?
``` Pain .Why? Persistent, recurrent episodes of severe pain Anorexia, nausea Constipation, flatulence Steatorrhea Diabetes ```
102
Evaluation of cp ?
or normal amylase and lipase Plain AXR CT may show calcified pancreas
103
Complications of cp ?
Exocrine insufficiency manifests as -weight loss and steatorrhea Endocrine insufficiency may result from islet cell destruction which leads to diabetes
104
what the hint for diagnosis for chronic pancreatitis ?
- steatorrhea present - trypsinogen level < 10 so Manage with low-fat diet and pancreatic enzyme supplements (Pancrease, Creon) *CREON is a prescription medicine used to treat people who cannot digest food normally because their pancreas does not make enough enzymes
105
management for chronic pancreatitis ?
- No cure . Symptomatic treatment. - Alcohol cessation may improve pain -Pain management critical but Narcotic dependency is common - Steatorrhea: Therapy involves limitation of fat intake and administration of adequate amounts of exogenous pancreatic enzyme preparations to provide at least 10% of normal lipolytic activity in the duodenum at the time that the food substrate is present - . surgery Patients with a dilated duct (>6 mm) are candidates for ductal drainage, with lateral pancreaticojejunostomy It is important to achieve adequate decompression of the enlarged pancreatic head and uncinate process during drainage procedures ن المهم تحقيق تخفيف الضغط الكافي لرأس البنكرياس
106
what's the indication of surgery in chronic pancreatits ? and hat we should consider ?
Pain is the primary indication for surgery. - to Selection of the best operation for a particular patient - consideration of the anatomy of the gland - preexisting endocrine or exocrine dysfunction, - postoperative endocrine or exocrine deficiency - compliance and the rehabilitative capacity of the patient, - postoperative pain relief.

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