Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BRS missed out > Gastro missed out questions > Flashcards

Gastro missed out questions Flashcards

1
Q

What mediates this - reflective relaxation?

A

Inhibitory noncholinergic nonadrenergic (NCNA) neurones of myenteric plexus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where does the oesophagus start and intersect the diagphram

A

C5 - T10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define Achalasia

A

Hypermotility of oesophagus due to loss of ganglion cells in Aurebach’s myenteric plexus in LOS wall
Leads to decreased activity of inhibitory NCNA neurones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

CREST syndrome

A
  • **Calcinosis- deposits of calcium in soft tissue
  • Raynaud’s phenomenon- constriction of peripheral blood vessels, can lead to problems with hands
  • Esophageal problems
  • Sclerodactyly- thickening of digits of hands and toes
  • Telangiectasia- dilated or broken blood vessels near surface of skin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is LOS pressure increased by?

A
  • Acetylcholine
  • Alpha adrenergic agonists
  • Hormones
  • Protein-rich food
  • Histamine
  • High intraabdominal pressure
  • PGF2alpha etc
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is LOS pressure decreased by?

A

VIP (vasoactive intestinal polypeptide)
- Beta adrenergic agonists
- hormones, dopamine
- NO
- PGI2
- PGE2
- chocolate
- acid gastric juice
- Smoking etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which regions of the hypothalamus detects change in osmolality?

A
  1. Organum vasculosum of the lamina terminalis (OVLT)
  2. Subfornical organ
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the functions of angiotenisn II in the renin- angiotensin- aldosterone pathway?

A

Thirst
ADH production
Aldosterone production
Vasoconstriction
H2O retention via potassium excretion and sodium chloride absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the function of aldosterone in the renin- angiotensin - aldosterone pathway?

A

H2O retention via potassium excretion and sodium chloride absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Outline the regions in the hypothalamus involved in appetite control.

A

Arcuate nucleus - location of POMC (inhibitory) and NPY/AGRP (stimulatory).
One of their terminal ends is in the paraventricular nucleus which regulates appetite.
Lateral hypothalamus - increase appetitie ( only orexigenic peptides)
Ventromedial hypothalamus - increase satiety ( decreasing appetite)
// Melanocortin system regulates food intake - decreases appeitie
Amygdala - emotiona and memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What do leptin act on?

A

Acts on cell receptors in arcuate and ventromedial nuclei-mediate feeding and thermogenesis energy expenditure

Made by adipocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the mechanism of leptin?

A

Acts on hypothalamus - decrease food intake, increase glucose and fat metablosim, increase energy expenditure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What gastrointestinal hormones are involved in appetite regulation?

A

Ghrelin- stimulates appetite and increases gastric emptying and Peptide tyrosine tyrosine (PYY) - inhibits

Secreted by enteroendochrine cells in the stomach, small bowel and pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Function of ghrelin

A

Increase appetitie
Increase gastric emptying , motility and acid secretion in the lead up to a meal
Stimulates NPY/AGRP. inhibits POMC
Reward, taste, sensation, circadian rhytmn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Function of peptide tyrosine tyrosine

A

Inhibit NPY/ AGRP
Stimulates POMC
Decrease appetite

Released by terminal ileum and colon in response to food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What blood result differentiates between severe and non severe c. diff?

A

WCC > 15, CRP > 150

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What infection affecting the colon is common with c.diff and what can be seen on examination?

A

Pseudomembranous colitis

Characteristic yellow-white plaques that form pseudomembranes on the mucosa

Confirmed on endoscopy +/- biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the indications for surgery following toxic megacolon?

A

-Colonic perforation
-Necrosis or full-thickness ischaemia
-Intra-abdominal hypertension or abdominal compartment syndrome
-Clinical signs of peritonitis or worsening abdominal examination despite adequate medical therapy
-End-organ failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ulcerative colitis classification

A

Mild

4 x BMs/day, no systemic toxicity, normal ESR/CRP, mild symptoms.

Moderate

> 4x BMs/day, mild anaemia, mild symptoms, minimal systemic toxicity, nutrition maintained and no weight loss.

Severe

> 6 BMs/day, severe symptoms, systemic toxicity, significant anaemia, increased ESR/CRP and weight loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Outline the mechanism, transmission, symptoms and diagnosis and treatment of CHOLERA.

A

Mechanism: Cholera - acute bacterial disease caused by Vibrio cholerae serogroups O1 & O139

Bacteria reaches small intestine → contact with epithelium & releases cholera enterotoxin.

Transmission:
Transmitted through faecal-oral route
Spreads via contaminated water & food.

Main symptoms :
Severe dehydration & watery diarrhoea

Other symptoms:
Vomiting, nausea & abdominal pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When dividing the surface anatomy of the abdominopelvic region into ninths what lines cross where?

A

Right & Left vertical - midclavicular lines

Top horizontal line - Transpyloric line

Bottom horizontal line - Interspinous line through the 2 ASIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the colicky nature of Ureter, Intestine, Billiary

A
  • Ureteric colic is defo colic- comes in waves- pain intensity gets high then drops
  • Intestinal colic is still colic but less painful than ureteric
  • Biliary colic doesn’t have to be true colic as it gets to a high intensity but then fluctuates at that high level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where does gallbladder (right hypochondriac region) pain radiate?

A

Through to the back and right- this happens in 50% of cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where does stomach, duodenum, pancreas (epigastrium) pain radiate?

A
  • Straight through to back- especially because pancreas and duodenum are retroperitoneal
  • People with pancreatic cancer present with back pain because tumour infiltrates posteriorly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where does tail of pancreas (left hypochondriac region) pain radiate?

A

Through to the back and the left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

S → Central then shifts to right iliac region

O → Gradual

C → Constant

R → No radiation

A → Nausea, anorexia, fever

T → No previous pain

E → Worse on movement

S → Dull ache

A

Appendicitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Murphy’s sign

A

Murphy’s sign is elicited in patients with acute cholecystitis by asking the patient to take in and hold a deep breath while palpating the right subcostal area. If pain occurs when the inflamed gallbladder comes into contact with the examiner’s hand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How do we manage peritonitis pre-operatively then operatively?

A
  • Put NG tube in to empty gastric contents to stop them leaking into abdomen
  • NBM or else anything that goes in will go through the hole
  • IV fluids
  • Antibiotics

Operatively

  • Identify aetiology of peritonitis (where hole is)
  • Eradication of peritoneal source of contamination
  • Peritoneal lavage and drainage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What treatments for gastric perforated ulcers are there?

A
  • Taylor’s approach- conservative treatment if they have localised peritonitis that seems to have sealed off itself and they’re not fit for surgery
  • Radical surgery- vagotomy, gastrectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Management principles of acute pancreatitis?

A
  • ABC
  • 4 principles of management:
    • Fluid resuscitation (IV fluids, urinary catheter, strict fluid balance monitoring)
    • Analgesia
    • Pancreatic rest (with or without nutritional support if prolonged recovery e.g. NJ feeding or PN)
    • Determine underlying cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Define malnutrition

A

A state in which deficiency, excess or imbalance, of energy, protein or other nutrients, results in a measurable adverse effect on body composition, function and clinical outcome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Causes of malnutrition (3)

A

Reduced intake

Malabsorption

Altered metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe altered metabolism cause of malnutrition

A

Cuthbertson et al. - There is a % decrease in energy expenditure following injury (shock) for about a day then the body enters a catabolic state to protect itself, the nutritional priority at this point would be covering metabolic needs. This lasts for a couple of days to a week, its at this point the body can now move to anabolic priority and nutrition can be focused to recovering muscle mass.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is used to diagnose malnutrition?

A

‘MUST’ calculator
Current weight, height (BMI)
Weight 3 months ago - percentage loss
Acute disease effect - acutely ill and/or no intake in past 5 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is involved in the dietician assessment of malnutrition?

A

Anthropometry
Body composition
Function
Biochemistry
Clinical
Dietary
Social
Physical
Requirements

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Indications of nutrition support

A

Malnourished =
BMI < 18.5 kg/m2 or
Unintentional weight loss >10 % past 3 - 6 / 12 or

BMI < 20 kg/m2 + unintentional weight loss > 5 % past 3 – 6 / 12.

  1. At risk of malnutrition =
    Have eaten little or nothing for > 5 days and / or are likely to eat little or nothing for the next 5 days or longer or

Have a poor absorptive capacity, and / or have high nutrient losses and/or have increased nutritional needs from causes such as catabolism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Algorithim for treatment of malnutrition

Is oral nutrition accessible and safe?
If YES?

A

a) Oral nutritional support

Dietetic counselling, dietary fortification, oral nutritional supplements, additional snacks –> Consider need for modified diet

b) But requires texture modification (e.g. dysphagia) –> SpLT

Finally - Regularly monitor intake

38
Q

Following oral nutrition if nutrition is inadequate what is the next step?

A

Enteral tube feeding

a) Short term 2 - 4 weeks –> fine bore naso enteral tube

b) long term > 4 weeks –> Long term placement such as gastrostomy

Finally - regularly monitor intake

39
Q

Algorithim for treatment of malnutrition

Is oral nutrition accessible and safe?
If NO and the GI tract is inaccessible or unsafe?

A

Parenteral nutrition

40
Q

. What are the complications associated with enteral feeding?

A

Mechanical: misplacement, blockage, buried bumper

Metabolic: hypergylcaemia, deranged electrolytes

GI: Aspiration, nasopharyngeal pain, laryngeal ulceration, vomiting, diarrhoea

41
Q

What are the complications associated with parenteral nutrition?

A

Metabolic - e.g hyperglycaemia
Catheter related infections
Mechanical - e.g pneuothorax

42
Q

What (syntheisised by the liver) can be used as a marker of poor prognosis in malnutrion?

A

Hypoalbuminaemia = poor prognosis.

43
Q

Consequences of RFS:

A

Arrhythmia, tachycardia, CHF → Cardiac arrest, sudden death

Respiratory depression

Encephalopathy, coma, seizures, rhabdomyolysis

Wernicke’s encephalopy

44
Q

Q. According to the National Institute for Health and Care Excellence (NICE), what are the criteria for defining the risk of RFS?

A

At risk:

Very little or no food intake for > 5 days

High risk:

 1 of the following:

BMI < 16 kg/m2

Unintentional weight loss > 15 % 3 – 6 /12

Very little / no nutrition > 10 days this

Low K+, Mg2+, PO4 prior to feeding

Or 2 of the following:
BMI < 18.5 kg/m2

Unintentional weight loss > 10 % 3 – 6 / 12

Very little / no nutrition > 5 days

PMHx alcohol abuse or drugs (insulin, chemotherapy, antacids, diuretics)

Extremely high risk:

BMI < 14 kg/m2

Negligible intake > 15 days

45
Q

Refeeding syndrome management

A

Administer thiamine 30 mins before and for the first ten days following trust policies

Correct and monitor electrolytes daily

Start 10- 20 kcal/ kg
Micronutrients from onset of feeding

Monitor fluid and minimise risk of fluid and Na+ overload

46
Q

GI Cancer Cell Names:
Glandular epithelium

Enteroendochrine cells

Interstital cells of cajal

Smooth Tissue

Adipose Tissue

A

Adenocarcinoma

Neuroendochrine Tumours

Gastrointestinal stroma tumours

Leimyoma

Liposarcoma

47
Q

Forms of colorectal cancer

A

Sporadic
Familial
Hereditary symptoms

Adenocarcinoma

48
Q

Risk for colorectal cancer

A

Past history
Colorectal cancer
Adenoma, ulcerative colitis, radiotherapy

Family history
1st degree relative < 55 yrs
Relatives with identified genetic predisposition
(e.g. FAP, HNPCC, Peutz-Jegher’s syndrome)

Diet/Environmental
carcinogenic foods
Smoking
Obesity
Socioeconomic status

49
Q

Colorectal cancer presentation depedning on location

A

Depending on location

⅔ in descending colon and rectum -

½ in sigmoid colon and rectum

Left sided & sigmoid colon - PR bleeding, mucus, Thin stool (late)

Rectal carcinoma - PR bleeding, mucus
Tenesmus ,Anal, perineal, sacral pain (late )

Caecal & right sided cancer - Iron deficiency anaemia (most common) ,Change of bowel habit (diarrhoea) ,Distal ileum obstruction (late) ,Palpable mass (late)

Bowel obstruction ( late)

50
Q

Colorectal presentation depending on invasion

A

Local invasion - Bladder symptoms
Female genital tract symptoms

Metastisis -
Liver (hepatic pain, jaundice)
Lung (cough)
Regional lymph nodes
Peritoneum -Sister Marie Joseph nodule

51
Q

Colorectal cancer - examination

A

Signs of primary cancer:
Abdominal mass
DRE: most <12cm dentate and reached by examining finger
Rigid sigmoidoscopy
Abdominal tenderness and distension – large bowel obstruction

Signs of metastasis and complications
Hepatomegaly (mets)
Monophonic wheeze
Bone pain

52
Q

Colorectal cancer investigations

A

Faecal occult blood - Guaiac test (Hemoccult)
Dietary restrictions – avoid red meat, melons, horse-radish, vitamin C & NSAIDs for 3 days before test

FIT (Faecal Immunochemical Test) - detects minute amounts of blood in faeces (faecal occult blood).

Blood tests
FBC: anaemia, haematinics – low ferritin
Tumour markers: CEA which is useful for monitoring
NOT diagnostic tool

53
Q

Colorectal cancer imaging

A

Colonoscopy
Can visualize lesions < 5mm

CT colonoscopy/colonography
Can visualize lesions > 5mm

MRI pelvis – Rectal Cancer
Depth of invasion, mesorectal lymph node involvement

CT Chest/Abdo/Pelvis
Staging prior to treatment

54
Q

Colorectal surgery Management

A

Primarily surgery
But also Stent/Radiotherapy/Chemotherapy

55
Q

Right sided obstructing colon cancer management

A

Resection and primary anastamosis

Hemicoloectomy +/- extension depedning on how close to transverse colon

Ileocaecal anastamosis

56
Q

Left sided obstructing colon cancer management

A

Hartmann’s procedure

Proximal end colostomy (LIF)

+/- Reversal in 6 months

Primary anastomosis

Intraoperative bowel lavage with primary anastomosis (10% leak)

Defunctioning ileostomy

Palliative stent

57
Q

Similarities with primary & secondary liver cancer, cholangiocarcinoma and gall bladder cancer

A

Low survival
Optimal Rx surgical excision with curative intent
Systemic chemotherapy ineffective

58
Q

Primary liver cancer called

A

Hepatocellular Carcinoma [HCC]

59
Q

Pancreatic cancer:

Most common type

Risk factors

A

pancreatic ductal adenocarcinoma (PDA)

Chronic pancreatitis
Diabtetes Mellitus II
Smoking
Occupation
Family History

60
Q

Pancreatic cancer pathogenesis

A

Pancreatic Intraepithelial Neoplasias (PanIN)

PDAs evolve through non-invasive neoplastic precursor lesions

PanINs are microscopic (<5 mm diameter) & not visible by pancreatic imaging

61
Q

Pancreatic cancer clinical presentation - carcinoma of the head

A

Jaundice
Palpable gall bladder
Weight loss - diabetes, malabsorption , anorexoa
Pain - epigastrium , radiates to back ( probs therefore irresectable)

Persistent vomiting - advanced
Gastrointestinal bleeding

62
Q

Pancreatic cancer clinical presentation - carcinoma of body and tail

A

Early stage asyptomatic

Weight loss and back pain

jaundice is uncommon
Vomiting may occur
Most unresectable at time of diagnosis

63
Q

Pancreatic cancer investigation

A

Tumour marker CA19-9 - falsely elevated in some pancreatic and hepatic disorders

Ultrasonography - liver metastis, bile duct dilation , pancreatic tumour

Dual-phase CT - predicts resectability (also MRI)

64
Q

Pancreatic cancer other investigations

A

MRCP - ductal images

ERCP - mostly for therapeutic purposes

EUS -detection of small tumours, fine needle aspirate

Laparoscopy & laparoscopic ultrasound - occult liver

Pet - occult metastisis

65
Q

Neuroendochrine tumours
Arise from

Associated with what genetic syndrome?

A

gastroenteropancreatic (GEP)

75% sporadic
25% genetic
Multiple Endocrine Neoplasia Type 1 (MEN1)

66
Q

Neuroendochrine tumour presentation

A

Most NETs are asymptomatic & incidental findings

OR

Secretion of hormones and metabolites e.g serotonin

Carcinoid syndrome:

Vasodilatation

Bronchoconstriction

↑ed intestinal motility

Endocardial fibrosis (PR & TR)

67
Q

NETS common site of actions and their names/ symtoms

A

Pancreas - insulinoma, glucagonoma

Pancreatic / Duodenal - gastrinoma

Entire GIT - VIPoma
Somatostatinoma

Midgut - most non functioning , or carcinoid syndrome

Hindgut - non functioning

68
Q

Neuroendochrine tumour diagnosis

A

Biochemical Assessment:
Chromogranin A is a secretory product of NETs
Other gut hormones - Measured in fasting state

Other screening: Calcium, PTH, prolactin, GH
24 hr urinary 5-HIAA (serotonin metabolite)

Imaging - the works

69
Q

Grading of GEP-NETs
( G3 - neuroendochrine carcinoma)

A

Grade Mitoses Ki-67 Index

G1 <2/10 H.P.F. </= 2%

G2 2-20/10 H.P.F. 3-20%

G3 >20/10 H.P.F. >20%

70
Q

Treatment for NETs

A

Curative resection (R0)
Cytoreductive resection (R1/R2)

And more not worth learning

71
Q

Frequency of liver mets in NETs ranked

A

Small intestine
Pancreas
Colon
Stomach
Rectum
Appendix

72
Q

What blood tests could we look at in response to acute abdomen? (5)

A

VBG
FBC
U & E
LFT + amylase
CRP

73
Q

Bowel ischaemia presentation

A

Sudden onset crampy abdominal pain
Severity of pain depends on the length and thickness of colon affected
Bloody, loose stool (currant jelly stools)
Fever, signs of septic shock

74
Q

Bowel ischaemia risk factors

A

Age >65 yr
Cardiac arrythmias (mainly AF), atherosclerosis
Hypercoagulation/thrombophilia
Vasculitis
Sickle cell disease
Profound shock causing hypotension

75
Q

Acute mesenteric ischaemia (SB) vs Ischaemic colitis (LB)

A

SB usually due to occlusive nature of thromboemboli vs LB which is due to non occulsive states such as low flow states or atherosclerosis

SB normally sudden onset vs LB normally gradual and slow

SB pain out of proportion to clinical signs vs LB moderate pain and tenderness

76
Q

Bowel ischaemia investigations

A

Bloods -
FBC: neutrophilic leukocytosis
VBG: Lactic acidosis

Imaging - CTAP/CT Angiogram
Detects:
Disrupted flow
Vascular stenosis
Pneumatosis intestinalis
Thumbprint sign

Endoscopy
For mild or moderate cases of ischaemic colitis

77
Q

Bowel ischaemia conservative management

A

Mild or moderate coliitis -
IV fluid resuscitation
Bowel rest
Broad-spectrum ABx
NG tube for decompression - in concurrent ileus
Anticoagulation
Treat/manage underlying cause
Serial abdominal examination and repeat imaging

78
Q

Bowel ischaemia surgical management
Indications

A

Small bowel ischaemia
Signs of peritonitis or sepsis
Haemodynamic instability
Massive bleeding
Fulminant colitis with toxic megacolon

79
Q

Bowel ischaemia surgical management

A

Exploratory laparotomy:
Resection of necrotic bowel +/- open surgical embolectomy
or mesenteric arterial bypass

Endovascular revascularisation:
Balloon angioplasty/thrombectomy
In patients without signs of ischaemia

80
Q

Acute appendicitis Investigations Bloods

A

FBC: neutrophilic leukocytosis
↑ed CRP

Urinalysis: possible mild pyuria/haematuria

Electrolyte imbalances in profound vomiting

81
Q

Acute Appendicitis Investigation Imaging

A

CT: gold standard in adults esp. if age > 50

USS: children/pregnancy/breastfeeding

MRI: in pregnancy if USS inconclusive

Diagnostic laparoscopy if inconclusive

82
Q

Alvarado score
What is it used for?
What does it describe?

What does the result mean?

A

Acute Appendicitis

RLQ tenderness ,Fever ( >37.3 degree celcius) ,Rebound tenderness ,Pain migration
Anorexia ,Nausea +/- vomiting ,WCC >10
Neutrophillia

Results:
</= 4 unlikely
5-6 Possibnle
>/= 7 Likely

83
Q

Acute appendicits conservative management

A

IV Fluids, Analgesia, IV or PO Antibiotics

In abscess, phlegmon or sealed perforation

Resuscitation + IV ABx +/- percutaneous drainage

Consider interval appendicectomy - CT drainage then 12 weeks later surgery

84
Q

Acute appendicitis surgical management

A

Laparoscopic vs Open appendicectomy

Laparoscopic:
Less pain, Lower incidence of surgical site infection, ↓ed length of hospital stay, Earlier return to work, Better quality of life scores

85
Q

How would you classify bowel obstruction?

A

Paralytic ( Adynamic)

Mechanical -
Speed of onset: acute, chronic, acute - on - chronic
Site - high or low
Nature - simple vs strangulating

86
Q

Small bowel obstruction aetiology

A

Adhesions
Neoplasia
Incarcerated hernia
Crohns disease
Other

87
Q

Large bowel obstruction aetiology

A

Colorectal carcinoma, Volvulus, Diverticulitis, Faecal implantation + more

88
Q

Features suggesting strangulation in bowel obstruction

A

Change in character of pain from colicky to continuous

Tachycardia

Pyrexia

Peritonism

Bowel sounds absent or reduced

Leucocytosis

↑ed C-reactive protein

89
Q

Common hernia sites

A

Inguinal and femoral hernias in groin as a result of defect in skin

Incisional hernias
Umbilical
Epigastric

90
Q
A

BRS missed out (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions