Abdominal Pain and Diarrhea Flashcards

1
Q

With somatic sensations it is easy to pinpoint which specific location the pain is occurring at.

A

But with visceral pain, the afferent nerves of the spinothalamic tracts are synapsing at multiple sites throughout the spinal cord so poor localization of the pain.

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2
Q

Which tract eventually alerts us to the effects of pain?

A

spinoreticular pathway

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3
Q

Pain sensation relayed to thalamus

Neurons project to cerebral cortex: pain ‘mapping’ done by somatosensory cortex in the thalamus

A

Descending fibers modulating pain are predominantly inhibitory

The inhibitory pathways originate in the cortex, limbic system with projections from midbrain and medulla

Fibers project on dorsal horn which leads to modification or control the afferent input from the gut

Efferent fibers descend down the cord through the spinal nerves which causes sympathetic and parasympathetic supply to the organ so that it could mediate the action (increase peristalsis, increase secretion)

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4
Q

Referred Pain is felt in areas remote from the diseased organs

A

Results when visceral afferent neurons & somatic afferent neurons from a different anatomic region converge on second order neurons in the spinal cord at the same spinal segment: central convergence

All spinal neurons that receive input from the viscera also receive input from the skin

Eventually you get sensitization that leads to hyperalgesia w. spasms (guarding rigidity)

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5
Q

What are the two classes of abdominal pain?

A

nociceptive and neuropathic

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6
Q

Nociceptive pain stimulates peripheral receptors. How would it manifest?

A

Mechanical: Stretch, distension

Injury: Inflammation, Ischemia

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7
Q

Neuropathic pain arises independently of nociceptor stimulation. It also presents as structural and functions changes in the pathway central or peripheral.
Give some examples

A

Diabetic neuropathy

Functional pain syndromes

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8
Q

Four pain patterns A,B,C,D

A

A: self-limited, relatively short period (gastroenteritis)

B: colicky pain (increases then decreases then increases then decreases)

C. Progressively worsening pain (appendicitis)

D. Catastrophic pain - sudden onset of very severe pain (ruptured aortic aneurysm)

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9
Q

Physical Exam for Peritonitis

A

‘quiet’ abdomen: diminished abdominal movements, loss of abdominothoracic breathing pattern

Cullen’s sign - bleeding below peritoneum
Frank Turner’s sign - bleeding below thigh
Distension/lump

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10
Q

Carnett Test for abdominal test for Peritonitis

A

To determine if abdominal pain is arising from the abdominal wall or has intraabdominal origin (visceral)

Pt asked to raise head this abdominal musculature tensed if greater tenderness on repeat palpation, test +, suggests abdominal wall pathology

If the tenderness persists, then it is abdominal wall

If it were visceral, after you tense up the abdominal wall the pain should decrease

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11
Q

Hypoactive or absent bowel sounds signifies

A

peritonitis

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12
Q

Hyperactive bowel sounds signify

A

enteritis, colitis, early part of obstruction

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13
Q

Peptic Ulcer presents as

A

epigastric, may radiate to back

Character: gnawing, burning, lasts for 1-3 hours
Gastric ulcer: food aggravates it
Duodenal ulcer: nocturnal, relieved by eating

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14
Q

Acute Pancreatitis presents as

A

Epigastric
Radiation: Back
Character: Deep boring, severe, usually last > 24 hours
Meals aggravate
Relieved by sitting upright
Nausea & vomiting usually + ; associated ileus

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15
Q

Intestinal pain presents as

A

Characteristic pain described as ‘colicky’ pain
Intermittent, crampy , poorly localized
Waxing and waning: becomes increasingly severe then passes off gradually to again return at intervals of few min

Small bowel obstruction-supra or periumbilical; colonic obstruction- infraumbilical with lumbar radiation

Proximal obstruction which causes vomiting (bilious) with some transient relief

Distal obstruction-distension, obstipation
With ischemia and necrosis, peritoneal signs supervene which colicky pain becomes sharp, localizable

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16
Q

Intestinal Angina is due to thrombosis presents as

A

Post prandial, occurs in individuals with insufficient blood flow to meetmesentericvisceral demands; + weight loss
Sitophobia: aversion to food

Tenesmus
Frequent and often painful inclination to evacuate the bowels with a feeling of incomplete evacuation

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17
Q

Rectal Pain presents as

A

pain in the rectal region that wakes patients up at night (tight rectal sphincter)

18
Q

Biliary Pain presents as

A

In its early stages,
Dull in epigastrium/RUQ with ongoing inflammation, becomes more localized in RUQ
Obstruction of cystic duct or bile duct increased intraluminal pressure repetitive biliary contractions
Sudden in onset, may persist with severe intensity 1-6 hours
Referred pain in RIGHT INFRASCAPULAR REGION

19
Q

Acute Cholecystitis

A

Pain persists if acute cholecystitis sets in
Acute cholecystitis leads to + Murphy’s sign

Boa’s sign: hyperesthesia in right infrascapular region that leads to phrenic nerve irritation, irritation of cutaneous nerves in referred dermatome

20
Q

Hepatic pain presents as

A

Deep lesions in the liver parenchyma are typically painless
Hepatic pain is produced by stretching of the Glisson capsule
-inflammation, vascular engorgement, rapidly expanding lesions underneath

21
Q

Splenic pain

A
LUQ; occurs when splenic enlargement causes stretching of capsule,
        splenic infarct (sickle cell)
22
Q

Appendicitis presents as PANT

A

Pain–> anorexia–> nausea–> tenderness
Initially pain is periumbilical, then with involvement of parietal peritoneum, becomes more localized in RLQ
McBurney’s point:

23
Q

Always remember

A

In a young female with acute abdominal pain, always r/o ectopic pregnancy
In upper abdominal pain, always keep cardiac and respiratory differentials in mind

24
Q

Causes of RLQ pain

A
appendicitis
terminal ileitis
Crohn's Disease
Tubovarian disorders
Ectopic pregnancy
Renal disorders
ureteric calculus
pyogenic sacroilitis
salpingitis
25
Q

Causes of RUQ pain

A

acute cholecystitis
biliary colic
hepatic inflammation or distention

26
Q

Causes of central abdominal pain

A

gastroenteritis
peptic ulcer disease
small bowel colic
Acute pancreatitis

27
Q

Causes of LUQ pain

A

splenic disorders

28
Q

Causes of LLQ pain

A

diverticulitis
colitis
sarcoilitis
tubovarian disorders

29
Q

Which syndrome predominantly affects women and is associated with depression and obesity

Pain is superficial, localized to small area with significant tenderness and dysesthesia

+Carnett sign

A

Chronic Abdominal Wall Pain Syndrome

30
Q

Median Arcuate Ligament Syndrome (MALS)/ Celiac artery compression syndrome

A

MAL formed at base of diaphragm where rt. and lt. diaphragmatic crura join near T12
Forms ant aspect of aortic hiatus
Typically median arcuate ligament arises slightly above origin of celiac artery
In MALS, ligament is anterior compression, irritation of celiac ganglion

31
Q

Superior Mesenteric Artery Syndrome

A

Compression of 3rd portion of duodenum by AA and overlying SMA
Normal angle between AA and SMA is 40-56- + retroperitoneal fat; loss acute angulation
Early satiety, nausea, vomiting, post pranadial abdominal pain, abdominal distension
Can present in acute or chronic form
Symptoms may improve after weight gain (hyperalimentation–> weight gain

32
Q

Irritable bowel Syndrome ROME criteria

A

Recurrent abdominal pain or discomfort ≥ 3 days/month in the last 3 months with 2 or more of the following:
Improvement with defecation
Onset associated with a change in frequency of stool
Onset associated with a change in form(appearance) of stool

33
Q

IBS has to do w

A

. afferent nerves

34
Q

Functional Abdominal Pain Syndrome(FAPS)
It is a subgroup of somatoform disorder
More common in women
Strong psychosocial component
H/O physical or sexual abuse often +
Typical pain is almost always there, constant, relatively unchanging in character, intensity , location
Nocturnal pain is typically considered ‘organic’…however, functional pain can also sometimes awaken from sleep

A

on exam you would see
Absence of autonomic features(tachycardia, diaphoresis)
Discrepancy between tenderness elicited with pressure from stethoscope and that from he examining hand

35
Q

Determinants of Intestinal Flux

A
  1. Balance between secretion and absorption maintained by endocrine, paracrine, neurocrine & immune mediators
  2. Neurotransmitters released by enteric neurons: VIP & Ach stimulate epithelial cells to secrete chloride
  3. Paracrine mediators released from local enteroendocrine cells : prostaglandins, histamine etc. secretagogues
  4. Bile salts leads to increases Cl- secretion
    Aldosterone leads to increases expression of transporters required for Na+ reabsorption in colon
  5. Motility leads to increases motility decreases absorption
  6. Inflammation: mediators increase secretion, decrease absorption
  7. Gut microbiome
36
Q

Pre-mucosal osmotic diarrhea is also known as intraluminal maldigestion manifests as lumenal

A

cholestasis or pancreatic insufficiency

37
Q

Mucosal osmotic diarrhea manifests as

A

enteropathies or due to drugs

38
Q

Post-mucosal osmotic diarrhea could be due to an

A

lymphangectasia (cannot get into lumen)

39
Q

examples of osmotic diarrhea

A
  1. Celiac disease
    Gluten enteropathy–> mucosal inflammation in proximal bowel villous atrophy decreased surface area
  2. Lactose intolerance
    Decreased lactase in surface absorptive cells–> lactose load fermentation osmotic load
  3. Infections
    Damage to brush border epithelium–> malabsorption
    Giardia, Cryptosporidium, Isospora, Strongyloides, MAI, Rotavirus
    Inflammatory infiltrate can cause lymphatic obstruction 4. Lymphangiectasia
    Whipple’s disease
  4. Drugs
  5. Thyrotoxicosis
40
Q

Secretory Diarrhea due to

A

tumors, bile salts,

41
Q

Acute infectious diarrhea

A

exotoxins, endotoxin-producing, invasive, C. diff gives negative blood cultures
Spurious diarrhea - due to impacted stool/constipations