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MRCS extra > Essential Facts > Flashcards

Essential Facts Flashcards

1
Q

SIRS Criteria

A
  • Temp >38 or <36
  • P >90
  • RR > 20
  • WCC >12 or <4
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2
Q

GLASGOW Score

A

Modified Glasgow - severity score:

  • P a02 < 7.9kPa
  • *A** ge > 55 years
  • *N** eutrophils > 15 x 10/l
  • *C** alcium < 2 mmol/l
  • *R** aised urea > 16 mmol/l
  • *E** nzyme (lactate dehydrogenase) > 600 units/l
  • *A** lbumin < 32 g/l
  • *S** ugar (glucose) > 10 mmol/l

> 3 positive criteria indicates severe pancreatitis.

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3
Q

Characteristics of ARDS

A

Acute condition characterized by:

bilateral pulmonary infiltrates
severe hypoxemia (PaO2/FiO2 ratio \< 200)

in the absence of evidence for cardiogenic pulmonary oedema (clinically or pulmonary capillary wedge pressure of less than 18 mm Hg).

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4
Q

Henderson Hasselbach Equation

A

CO2 + H2O HCO3- + H+

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5
Q

Anion Gap

A

(Na + K) - (HCO3- + Cl)

(Normal Range 12 +/- 2)

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6
Q

Normal Infrarenal Aortic Diameter

A

2cm

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7
Q

When to consider AAA for repair

A

>4.5cm or growing >1cm per year

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8
Q

Follow up for AAA

A

If < 3cm require no further follow up
3-4cm = annual USS
4-5.4cm = 6 monthly USS
>5.5 cm = immediate referral for repair

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9
Q

Breast Screening

A

Three yearly screening to all females 50 - 70y

(Currently being extended 47 to 73y)

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10
Q

Hormonal Therapy in Breast Cancer

A

Oestrogen dependant in 70% of cases

  • *Pre-menopausal:** Tamoxifen for five years (Selective oestrogen receptor modulator)
  • *Post-menopausal:** Aromatase inhibitors (eg Anastrazole) - block peripheral conversion only
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11
Q

Branchial cyst location

A

Anterior Triangle

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12
Q

Cystic Hygroma Location

A

Posterior Traingle

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13
Q

CVP Trace

A

ACXVY
A - Atrial Contraction
C - Tricuspid closure
X - Atrial relaxation
V - Venous return
Y - Opening of tricuspid

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14
Q

Surface area for burns

A

Rule of nines - Head, Arms, half leg, half torso 9% Genitals 1%
Hand - Patient’s hand = ~1%

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15
Q

Parkland Formula

A

4 x wt x surface area
Half over 8 hours
Half over 16 hours
Note: timer starts from time of burn, not time of assessment - inc rate of resuscitation appropriately.

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16
Q

Charcot’s traid

A

Fever, Jaundice and RUQ pain

(Suggests ascending cholangitits)

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17
Q

Indications for central line

A

Monitoring fluid balance / resuscitation
TPN
Certain medication infusions
Failed peripheral access
Haemodialysis
Transvenous cardiac pacing

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18
Q

Hartmann’s Contents

A

Na 131,

K 5,

Cl 111,

Ca 2,

Bicarb (as lactate) 29

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19
Q

Normal Saline Contents

A

Na 150,

Cl 150

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20
Q

Formula for MAP

A

MAP = (CO x SVR) + CVP

Or Estimated:
MAP = ((SBP +DBP) + DBP) / 3

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21
Q

Distribution of body fluids

A

1/3 Extra cellular
25% Intravascular
75% Interstitial
2/3 Inta-cellular

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22
Q

ECG Axis

A

Normal: -30deg to +90deg

Leads 1+2 both positive = Normal
Lead 1 positive, Lead 2/3 negative = Left axis deviation
Lead 1 negative = Right axis deviation

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23
Q

Pain transmition pathway / fibres

A

Sharp pain - A-delta fibres
Dull pain - C-fibres
Spinothalamic tract

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24
Q

Classification of blood loss

A

Class % P BP RR UO Mental

1 <15 <100 Norm <20 >30ml Anxious

2 15-30 <120 Wide PP <30 <30ml Anxious

3 30-40 <140 Red. <40 <15ml Confused

4 40+ >135 Red >35 Nil Lethargic

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25
Q

Anterior Pituitary Hormones

A

ACTH

TH

LH

FSH

GH

Prolactin

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26
Q

Posterior Pituitary Hormones

A

Oxytoncin

ADH

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27
Q

Parotid Gland Neoplasias

A

80% benign. (Pleomorphic adenoma (70%), Warthin’s tumor)
15% malignant. (Mucoepidermoid carcinoma, adenoid cystic carcinoma) - Facial nerve palsy suggests malignancy.

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28
Q

FAP + Gardner’s Syndrome

A

Mutation of APC gene (80% cases) - AUTOSOMAL DOMINANT

Predisposes to hundreds of adenomatous polyps. 100% risk GI Ca by 40y. Associated with small bowel polyps and mandibular osteomas.

Gardner syndrome (type of FAP): Associated with FAP - Osteomas of skull, epidermoid cyst, multiple desmoid tumours

Screening: Annual colonscopy from age of 15.

Assoc. with Duodenal polyps (90%), Gastric fundal polyps (50%)

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29
Q

Peutz-Jegher’s Syndrome

A

AUTOSOMAL DOMINANT - mutation on chromosome 19

Multiple hamartomatous polyps -> episodic obstruction and intussception.

Increased risk of GI cancers - Colorectal 20%. Increased risk of breast, ovarian, cervical, pancreatic

Assoc. Hyperpigmented macules on mouth and oral mucosa

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30
Q

HNPCC

A

HNPCC / Lynch syndrome

Germline mutations of DNA mismatch repair genes (MMR)

Colo rectal cancer 30-70%
Endometrial cancer 30-70%
Gastric cancer 5-10%
Scanty colonic polyps may be present
Colonic tumours likely to be right sided and mucinous

Colonoscopy every 1-2 years from age 25
Consideration of prophylactic surgery

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31
Q

MYH associated polyposis

A

mutation of mut Y human homologue (MYH) on chromosome 1p,

Recessive pattern

Multiple colonic polyps
Later onset right sided cancers more common than in FAP
100% cancer risk by age 60

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32
Q

Stages of organ rejection

A

Hyper-acute
Due to presence of recipient anti-bodies. Kidney swells and becomes necrotic, requires nephrectomy.

Acute
T-cell mediated diffuse lymphocytic infiltration. Reversible with high dose steroids

Chronic
Humoral system responsible for graft fibrosis and atrophy.

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33
Q

Testicular Ca

A
  • Germ Cell Tumours
  • Seminoma
  • Non-Seminomatous
  • Teratoma
  • Embryonal Carcinoma
  • Choriocarcinoma
  • Yolk Sac Tumour
  • Mixed Germ Cell Tumour
  • Non Germ Cell
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34
Q

Seminoma

A

Peak Age - 30-40
Placental Alk Phos
Radiotherapy effective (In effective for all non-seminomas)
B-HCG and lactate for monitoring following treatment

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35
Q

Teratoma

A

Peak Age 20 - 30
markers: B-HCG, CEA, AFP (Also found in HCC)

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36
Q

Melanoma Margins

A

<0.75mm = 1cm margin
< 1mm = 2cm
> 1mm = 3cm

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37
Q

Primary / Secondary / Tertiary healing

A

Primary healing
Wound closed within hours of formation, usually with sutures or clips

Secondary Healing
Left open without formal closure - spontaneous closure via contraction and re-epithelialisation

Tertiary Healing
Initial debridement with normal closure at a later date.

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38
Q

Vaccines required post splenectomy

A

Pneumococcal
H. Influenza B
Meningococcal

Flu

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39
Q

Duke’s Staging (and 5yr survivals)

A

A - Confined to tumour wall (95 - 100%)
B - Through bowel wall (65 - 75%)
C - Lymph node Mets (30 - 40%)
D - Distant mets (5 - 10%)

Nb Modified:

C1 = Upper LN not involved

C2 = Upper LN is involved

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40
Q

TNM Staging

A

Tis - Mucosa
T1 - Submucosa
T2 - Muscularis
T3 - Serosa
T4 - Adjacent Organs
N1 - <=3
N2 - > 3

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41
Q

Virchow’s Triad

A

Abnormal blood flow
Hypercoagulable state
Endothelial Injury

Causes of thrombus

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42
Q

MEN

A

I - Pancreatic (usually gastrinoma), Parathyroid (hyperplasia), Pituitary (usually prolactinoma)
IIa - Phaeochromocytoma, Parathyroid adenoma, Medullary Thyroid Ca
IIb - As IIa with Marfanoid features + Mucosal Neuromatosis

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43
Q

AFP Associations

A

Hepatocellular Carcinoma, Teratoma

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44
Q

CEA Associations

A

Colon, Teratoma

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45
Q

PSA Associations

A

Prostate

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46
Q

CA 125 Associations

A

Ovarian

47
Q

CA 19-9 Associations

A

Pancreatic

48
Q

B-HCG Associations

A

Teratoma

49
Q

Placental Alk Phos Associations

A

Seminoma

50
Q

Autograft

A

Graft from host

eg skin grafting

51
Q

Allograft

A

Transplant between two individuals who are not genetically identicle

52
Q

Isograft

A

Transplant between genetically identicle individuals

53
Q

Xenograft

A

Transplant between species

54
Q

Discuss the role of Parathyroid hormone?

A

Parathyroid Hormone: Increases serum calcium.
Causes osteoclasts to reabsorb calcium from bones (bodys main Ca store)
Increases reabsorption of Ca in the kidneys but decreases the reabsorption of Ph.
Activates Vit D which increases the reabsorption of Ca in the intestine.

NB as serum calcium levels fall levels of PTH rise

55
Q

What is the role of Calcitonin?

A

Produced by Thyroid C cells

Inhibits osteoclast activity in the bone.
Stimulates osteoblast activity.
Inhibits reabsorption of Ca in the Kidney therefore more will be present in the urine.
Inhibits reabsorption of Ca in the intestine.

Therefore overall effect decreases plasma calcium and phosphate
Can be used to treat osteoporosis and hypercalcaemia

56
Q

What is the role of Vitamin D?

A
  • Photoactivation (in the skin) is the primary source of Vitamin D.
  • It is converted to active form in the liver and kidney.
  • This increases:
    • Gut calcium absorption
    • Bone calcification
    • Bone reabsorption
  • Regulation is by PTH, phosphate and feedback inhibition.
  • Increases plasma calcium and phosphate
57
Q

What are the causes of raised serum calcium?

A

Look at Serum Calcium and Serum Phosphate
& Albumin

Albumin ↑ & Serum Calcium raised = Dehydration

Serum Phosphate low and Calcium ↑:
PTH mediated hypercalcaemia:
Serum calcium ↑, PTH not suppressed
Primary hyperparathyroidism (most common cause) - is a single adenoma in 90% cases

Serum phosphate ↑Calcium ↑ PTH LOW
Non PTH mediated hypercalaemia:
Bone metastasis (from breast, kidney, lung, thyroid, prostate)
Granulomatous conditions (sarcoidosis/TB)
Endocrine: Thyrotoxicosis, primary adrenal insufficiency
Iatrogenic: Thiazide diuretics (reduces calicum excretion), Vit D and A supplements
Familial: Familial Hypocalciuric hypercalcaemia

58
Q

What is primary hyperparathyroidism?

A

Due to single adenomas (>80%)

Carcinoma is rare

Involvement of multiple parathyroid adenomas also rare, may be part of familial syndromes eg MEN type 1 or 2a

Hypercalcaemia
BP is raised (so check calcium everyone BP)

59
Q

Clinical presentation of 1° hyperparathyroidism

A
  • Females over 50 y/o
  • Polyuria and polydispsia, leads to acute dehydration
  • Renal colic ‘Stones’
  • Dyspepsia and peptic ulceration ‘Abdominal Groans’
  • Depression ‘Moans’
  • Bone pain ‘Bones’
  • Lethargy
  • Anorexia and nausea
  • Constipation
  • Drowsiness and impaired cognitive function
60
Q

Laboratory features of 1° hyperparathyroidism

A
  • Several fasting serum calcium and phosphate samples should be performed
  • In primary hyperparathyroidism:
    • Increased Ca2+
    • Decreased phosphate
    • Normal or elevated PTH levels during hypercalcaemia.
  • Often mild hyperchloreamic acidosis (needs no treatment).
61
Q

Causes of 2° hyperparathyroidism

A
  • Parathyroid hyperplasia is a response to low blood calcium due to:
    • Chronic renal failure
    • Malabsorption
    • Osteomalacia & Rickets (Vit D deficiency)
  • Leads to decreased Ca2+, and increased PTH:
62
Q

What type of Cancers are MEN assoc with?

A

MEN 1 (Werner’s syndrome)

  • Primary hyperparathyroidism
  • Pituitary tumours
  • Pancreatic neuro-endocrine tumours (e.g. insulinoma, gastrinoma)

MEN 2 (Sipple’s syndrome)

  • Primary hyperparathyroidism
  • Medullary carcinoma of thyroid
  • Phaeochromocytoma
  • In addition, in MEN 2b syndrome there are phenotypic changes(including marfanoid habitus, skeletal abnormalities, abnormaldental enamel, multiple mucosal neuromas)​
63
Q

How does hypercalcaemia present

A

“Stones, Bones, Groans, Thrones and Psychiatric Overtones”

  • Stones (renal or biliary)
  • Bones (bone pain)
  • Groans (abdominal pain, nausea and vomiting)
  • Thrones (polyuria) resulting in dehydration
  • Psychiatric overtones (Depression 30–40%, anxiety, cognitive dysfunction, insomnia, coma)
64
Q

Acute Mx of hypercalcaemia

A

Investigations:

  • Measure U&E’s, Mg2+, creatinine, Ca2+, PO43-, alk phos, PTH
  • CXR and CT for metastases,
  • Abdominal US for intra-abdominal malignancy if symptoms

Management:

  • Rehydration with normal saline
    • To replace as much as a 4-6 L deficit
    • Moniter if renal failure / CCF
  • Bisphosphonates IV
    • Causes a fall in calcium which is maximal at 2-3 days and lasts a few weeks
65
Q

What are the causes of hypocalcaemia?

A

Most common: low albumin (↓Albumin → ↓Ca2+ ) as approx. 40% Calcium is bound to Albumin

Low PTH levels:
Hypoparathyroidism (frequently following surgery, radiotherapy or infiltartion e.g sarcoidosis or amyloidosis).

High PTH levels:
Vitamin D deficiency or abnormal metabolism.
Hypomagnesaemia (causing PTH resistance)

Other causes:
Renal failure (no renal reabsorption)
Medication.
Acute pancreatitis.

66
Q

Clinical features of Hypocacaemia

A

Tetany (intermittent muscle spasms)

  • Chvostek’s sign - gentle tapping over the facial nerve in the parotid causes twitching of the facial muscles.
  • Trousseau’s sign - inflation of the BP cuff above systolic blood pressure for 3 minute induces carpal spasm of the fingers and wrist.
  • Note: Mg2+ depletion can also be a cause of tetany.

Pneumonic SPASMODIC

  • *S**pasms (Trousseau’s sign)
  • *P**erioral Paresthesia
  • *A**nxious
  • *S**eizures
  • *M**uscle tone increased in SM (colic, wheezing)
  • *O**rientation impaired
  • *D**ermatitis
  • *I**mpetigo
  • *C**hvosteks sign
67
Q

Describe what symptoms would be seen total anterior circulation and a partial anterior circulation stroke?

A

Higher cortical dysfunction (agnosia, neglect, dysphasia)
Hemianopia
Motor or sensory deficit

Note: hemianopia is on the same side as the hemiparesis
The brain lesion will be on the other side eg if LEFT sided stroke will cause a right sided heminopia and right sided hemiparesis

In a total anterior stroke all three are present in a partial 2 of the 3 are present.

68
Q

Describe what symptoms would be seen in a posterior circulation stroke?

A

Isolated hemiapnopia
OR
Cerebellar ataxia
OR
Cranial nn lesions

69
Q

Describe what symptoms would be seen in a lacunar stroke?

A

One motor or sensory deficit.

70
Q

What is the name used to classify strokes?

A

Bamford classification.

Splits different strokes up into TACS, PACS, POCS and Lacunar based on the symptoms.

71
Q

Which is the most serious stroke you can have and what is the 1 year mortality for the different strokes?

A

Right TACS as it will effect the left dominant hemisphere.

TACS 60%
PACS 15%
LACS 10%
Posterior circulation 20%

72
Q

Types of Colon Resection

A
73
Q

First Pharyngeal Arch

A
  • *1st Arch: a Massive list of M’s**
  • *Nerve:** Maxillary and Mandibular nerves

Artery: Maxillary artery

  • *Cartilage: M**eckel’s Cartilage
  • Mandible + sphenoMandibular ligament
  • Malleus + Incus
  • *Muscles: MAT x 2**
  • Muscles of Mastication
  • Mylohyoid
  • Anterior belly of digastric
  • Anterior 2/3 of tongue
  • Tensor veli palatini
  • Tensor tympani
74
Q

Second Pharyngeal Arch

A
  • *2nd arch: Second**
  • *Nerve**: Seventh nerve (facial nerve)

Artery: Stapedial artery and hyoid artery

  • *Cartilage:**
  • Stapes
  • Styloid
  • Stylohyoid ligament
  • leSSer horn of hyoid
  • *Muscles:**
  • Muscles of facial expression (Smiling)
  • Stapedius
  • Stylohyoid
  • poSSterior belly of digastric
75
Q

Third Pharyngeal Arch

A

3rd arch: think Glossopharyngeal nerve

  • *Nerve:**
  • Glossopharyngeal nerve
  • *Cartilage:**
  • Greater horn of hyoid
  • *Muscle:**
  • Stylopharyngeus

Common and internal CAROTID

76
Q

4th Pharyngeal Arch

A

4th Arch: Swallowing + The exceptions to the 6th arch below

Nerve: Superior Laryngeal (branch of vagus)

  • *Cartilage:**
  • Thyroid cartilage
  • *Muscles:**
  • Pharyngeal constrictors
  • Levator veli palatini
  • Cricothyroid

R Subclavian artery and Left aortic arch

77
Q

6th Pharyngeal arch

A

6th Arch: Speaking (Laryngeal)

Nerve: Recurrent laryngeal (branch of vagus)

Cartilage: All laryngeal cartilages except thyroid cartilage

Muscles: All instrinsic laryngeal muscles except cricothyroid

R & L pulmonary artery and ductus arteriosus

78
Q

Fibroadenoma

A

18-25 they constitute up to 60% of all palpable breast lesions

<3cm - a policy of watchful waiting without biopsy may be adopted.

>4cm - core biopsy to exclude a phyllodes tumour.

The natural history of fibroadenomas is that 10% will increase in size, 30% regress and the remainder stay the same.

79
Q

Breast Cysts

A

Palpable cysts constitute 15% of all breast lumps. They occur most frequently in perimenopausal females and are caused by distended and involuted lobules.

imaging they will usually show a “halo appearance” on mammography. Ultrasound will confirm the fluid filled nature of the cyst

80
Q

What is a fibroadenoma?

A

A benign local proliferation of breast ducts and stroma

Ages 25-35 years

Macroscopically:
1-4cm in diameter
Firm, rubbery, well circumscribed lesions
Mobile

1/3 regress
1/3 stay the same
1/3 get bigger

81
Q

What is the most frequent disorder of the female breast, what proportion of women have it & what changes are seen?

A

Fibrocystic change

Present in 40% women
10% all women present with clinical symptoms

Hyperplastic overgrowth of components of the mammary unit ie lobules, ductules and stroma

If unequal growth of the epithelial and stromal elements get fibroadenoisis

82
Q

How does fibroadenosis present?

A

Palpable thickening & nodularity of breast tissue
Tissue is rubbery in texture
Varies in size with stage of hormonal cycle

May also result in development of a single breast lump

MUST be distinguished from malignancy

83
Q

How does carcinoma of the breast present?

A

Affects 1 in 12 women, uncommon in men.

Characteristically: Irregular outline
Often Painless
Firm or Hard

May be within the breast tissue or extend into overlying tissue.

84
Q

What are the different types of skin changes commonly seen in breast disease?

A

Dimpling skin but retraction skin mobile over tumour suggests benign disease

Skin may be indrawn due to infiltratio of dermis by tumour

Fixed to skin → malignant disease

Tethered to chest wall fixed when pectoral muscle contracted

PEAU D’ORANGE → obstruction intramammary lymphatics resulting in lymphoedema of the breast.
Skin attached at hair follicles but swollen inbetween

85
Q

What are the different types of nipple inversion that are seen?

A

Benign nipple inversion (symmetrical )

Inversion

Nipple retraction → malignant disease asymmetrical and distorting

NB always investigate nipple discharge

86
Q

What are the types of non invasive cancer of the breast

A

Non-invasive ductal carcinoma in situ (5%)
Pre-malignant

Non-invasive lobular carcinoma in situ
Histological finding rather than a mass
Pre-malignant but high chance of malignancy
NB this risk is present for both breasts, not just affected breast

87
Q

What are the types of invasive carcinoma of the breast?

A

ductal pure, ductal mixed
lobular
tubular
mucoid
medullary

88
Q

What is the most common carcinoma of the breast?

A

Invasive ductal carcinoma (70%)

89
Q

What is the 2nd most common type of breast cancer

A

Invasive lobular carcinoma
High frequency of bilateral breast involvement compared to other tumour types

90
Q

What are the risk factors for Carcinoma of the breast?

A

Familial breast cancer (5% cases) (BRACA1 & BRACA2)

Geographical - developed countries

Proliferative breast disease eg atypical duct hyperplasia

Uniterrupted Oestrogen exposure:
Early onset menarche
Late birth first child / nulliparous state
Late menopause
Exogenous hormones

91
Q

How is the diagnosis of a breast lump made?

A

Triple Assesment:

  1. Clinical Examination
  2. Radiology: USS for < 35 y/o, Mammography & USS for > 35 y/o
  3. Histology / cytology:

​​Cystic lump → FNA or core biopsy
Solid lump → Core biopsy

92
Q

Tx of fibroadenomas

A

All large fibroadenomas should be excised

Clinically apparent lesions in postmenopausal period should also be excised

93
Q

Tx for Cysts in breast

A

Require no Tx unless they are associated with persistent lump or cyst fluid is blood stained

USS can help to identify cysts that should be excised

94
Q

What is the nottingham prognosis index

A

Nottingham prognostic index:
Based on 3 prognostic factors clinically stages breast tumours
Tumour size (cm x 0.2)
Lymph node stage (1 = node negative, 2 = 1-3 metastatic nodes, 3 = 4+ metastatic nodes)
Histological grade (1-3 for good, moderate, poor)

Score < 3.4 indicated good prognosis
Score 3.4-5.4 moderately good prognosis
Score > 5.4 poor prognosis

95
Q

How is staging done once breast cancer has been confirmed?

A

TNM
Early cancer: 1-2
Advanced breast cancer: 3-4

T
T0 – carcinoma in situ or microinvasion
T1 – tumour < 2cm
T2 – tumour 2-5cm
T3 – tumour > 5cm
T4 – Overlying skin or underlying muscle attachment

N
N0 – no axillary nodal involvement
N1 – free axillary nodes (histologically less than 3 nodes involved)
N2 – more than 3 nodes involved or fixed axillary nodes
N3 – Supraclavicular nodes involved

M
M0 – no metastasis
M1 – metastatic disease present

96
Q

What further investigations need to be perfored in more advanced cases?

A

CAT scan of lung & liver

Bone scan

Blood tests: FBC, LFTs, carcinoembryonic antigen (Ca15.3)

97
Q

Tx for early breast cancer

A

Local Tx:
Lumpectomy + Radiotherapy
Simple mastectomy

Tx for axillary lymph nodes:
Axillary dissection
Radiotherapy to the axilla

Prevention systemic spread:
Tamoxifen (Oestrogen receptor blocker)
Adjuvant chemotherapy

98
Q

Tx for late breast cancer

A

Distant spread at time of diagnosis

Treatment of late breast cancer is usually palliative and mostly medical

Local treatment is directed at controlling local recurrence: lumpectomy/mastectomy/radiotherapy

Distant metastases: radiotherapy to relieve pain from bony metastases; chemotherapy (tamoxifen, cytotoxics, aminoglutethimide) to control tumour load

99
Q

Current survival rates of treated breast cancer

A

Early cancer: overall 80% 10-year survival rate

Advanced cancer: poor, only 30-40% respond to treatment with mean survival of 2 years, by which time the non-responders have usually died

If metastasis are present then only 15% of patients will survive for 5 years; life expectancy (50% mortality) is 2-3 years.

100
Q

How should nipple discharge be investigated

A

Requires investigation if blood stained

Important to determine if the discharge is from multiple ducts or a single duct

If bilateral and milky → serum prolactin (rule out physiological discharge)

101
Q

What does a unilateral blood stained nipple discharge mean?

A

Usually Intraductal Papilloma (usually benign)

Follow up with Triple Assesment

Confirm presence of blood in discharge with dipstick

102
Q

What is the National Breast Screening programme?

A

women aged between 50 and 70 for screening every 3 years

2 seperate mammograms performed.

If any abnormalities suspected then patients are called back within 2 weeks

103
Q

What is Pagets disease?

A

Skin: The first symptom is usually an eczema-like rash. The skin of the nipple and areola may be red, itchy and inflamed

Discharge. straw-colored or bloody

Some women have a burning sensation

104
Q

Deep Tendon Reflexes

A
107
Q

What are some examples of obstructive diseases and the process behind the results

A

Asthma, bronchitis and empysema

Characterised by Airway Narrowing -> maximum expiratory flow is limited by dynamic compression of small intrathoracic airways -> limiting the volume that can be expired

-> Hyperinflation of the chest which can become extreme if elastic recoil is also lost due to parenchymal destruction, as in empysema

108
Q

What are some examples of restrictive lung disease and what is the pathology behind them

A

Diseases which causes lung inflammation &/or scarring and fibrosis

fibrosing alveolitis, scoliosis

-> loss of lung volume with normal expiratory flow rates

Gas exchange is impaired both by parenchymal destruction (empysema) & by interstitial disease which interupts venitlation and perfusion matching

109
Q

What spirometry results would you expect in the following conditions Asthma, Chronic bronchitis, emphysema, pulmonary fibrosis?

A
110
Q

What would you expect the spirometry to show in restricted and obstructive spirometry?

A
111
Q

What are the findings in airway obstruction

A

FEV1 is disproportionately reduced in airflow obstruction resulting in FEV1/VC ratios of less than 70%.

When obstruction is seen spirometry should be repeated following inhalation of SABA

112
Q

How can lung volume be measured?

A

Dilution of an inert gas (usually helium)

Measures the vilume of intrathoracic gas which mixes quickly with tidal intrathoracic gas volume including poorly ventilated areas

Can also have 0.3% CO which is used with a breath hold test to look at exchange of gas

THis is termed KCO (gas transfer per unit lung volume)

113
Q

Findings in Cardiogenic Shock

A

e.g. MI, valve abnormality

increased SVR (vasoconstriction in response to low BP)
increased HR (sympathetic response)
decreased cardiac output
decreased blood pressure

114
Q

Findings in Hypovolaemic shock

A
  • *blood volume depletion**
    e. g. haemorrhage, vomiting, diarrhoea, dehydration, third-space losses during major operations

increased SVR
increased HR
decreased cardiac output
decreased blood pressure

115
Q

Septic Shock

A

Septic shock:
occurs when the peripheral vascular dilatation causes a fall in SVR
similar response may occur in anaphylactic shock, neurogenic shock

reduced SVR (due to extensive cytokine release)
increased HR
normal/increased cardiac output
decreased blood pressure

116
Q

Mx of Anaphylaxis - Adults

A

Adrenaline: 500 mcg (0.5ml 1 in 1,000)

Hydrocortisone: 200 mg

Chlorphenamine: 10mg

MRCS extra (5 decks)

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