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Pathology combined Flashcards

all that is highlighted in lectures

1
Q

What is aneurysm?

A

Localized dilation of a vessel

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2
Q

What are the types of aneurysm?

A

Fusiform: around the circumference Saccular: bulging from the side

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3
Q

What is the Aetiology of aneurysm

A

Artherosclerosis Hypertension infection connective tissue disorder

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4
Q

what are the complications of aneurysm

A

dilation and rupture thrombosis thromboembolism

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5
Q

What is the Clinical presentation of aneurysm

A

Male hypertensive smoker 50+ acute abdominal pain shock

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6
Q

What are the risk factors for GORD?

A

***Decreased tone of LOS Impaired musculoskeletal defences Increased IAP

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7
Q

What is barret’s mucosa?

A

*****squamous epithelium replaced by columnar epithileum

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8
Q

Clinical features for Garrets mucosa?

A

****Heartburn dyspepsia Dysphagia

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9
Q

What is the Aetiology for acute gastritis?

A

******Infective agents: Salmonella, E. Coli Direct damage: alcohol, NSAIDs Inhibition of mucosal replacement: chemotherapy, radiotherapy

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10
Q

Aetiology of chronic gastritis

A

****infection H pilori autoimune gastritis vitamin B12 deficiency

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11
Q

What are the sites for ulcers?

A

**Duodenal ulcers are more common than gastric - 4:1. Duodenal ulcers: D1, Gastric ulcers: lesser curvature

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12
Q

Clinical features for ulcers?

A

Epigastric pain Anorexia, dyspepsia, nausea, vomiting

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13
Q

What are complications of ulcers?

A

pyloric stenosis Iron deficiency anaemia, melena, haematemesis

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14
Q

Management for ulcers?

A

H.pilory infection: amoxicillin clarithromycin metronidazole

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15
Q

What is celiac disease

A

hypersensitivity reaction to gluten or its peptide derivative, GLIADIN

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16
Q

What is the bowel most affected by celiac disease?

A

duodenal jejunal flexure

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17
Q

what are the complications for celiac?

A

Generalised malabsorption: Ulcerative jejuno-ileitis: Increased risk of GIT cancers Skin disorders

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18
Q

Clinical features celiac?

A

Children: Irritability, failure to thrive, abdominal distension Voluminous, pale stool Adults: Weight loss, diarrhoea Abdominal discomfort, excessive flatus Fatigue Amenorrhea

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19
Q

Management for celiac

A

patient education and dietary modification

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20
Q

Why pathologies cause jaundice?

A

liver disease Extra hepatic disorder caused by elevated BILIRUBIN

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21
Q

How does bilirubin metabolism work?

A

Bilirubin is a pigment made during the normal breakdown of RBCs into HEME and GLOBIN

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22
Q

What are the classification or different types of jaundice?

A
  • Haemolitic jaundice: RBC destruction - hepatic jaundice: impaired hepatocyte disfunction (hepatitis, cirrhosis) - Neaonatal jaundice: babies - Cholestatic jaundice: obstruction of bile ducts
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23
Q

What is viral hepatitis?

A

Epson barr virus

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24
Q

how does hepatitis A work?

A

•Transmission: Faecal-oral route •Severity: Usually mild, worse in older patients •Chronicity: Very rare •Vaccination: Yes

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25
Q

how does hepatitis B work?

A

•Transmission: Parenteral, sexual contact, perinatal •Severity: Mild to severe (mortality ~10%) •Chronicity: Common •Vaccination: Yes

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26
Q

how does hepatitis C work?

A

•Transmission: Parenteral, perinatal, possibly sexual •Severity: Usually mild •Chronicity: Very common •Vaccination: Not available

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27
Q

What is the management for Hepatitis?

A

There is no specific treatment. - aim to reduce spread.

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28
Q

What is alcoholic liver disease?

A

Induction of oxidases

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29
Q

Describe the 1st stage of alcoholic liver disease (fatty liver)?

A

STAGE 1: FATTY LIVER hepatomegaly

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30
Q

Describe the 2nd stage of alcoholic liver disease (alcoholic hepatitis)?

A

STAGE 2: ALCOHOLIC HEPATITIS hepatocyte necrosis - cell death •Clinical features: tender hepatomegaly, fever, jaundice, ascites complication ****encephalonopathy

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31
Q

Describe the 3th stage of alcoholic liver disease (cirrhosis)?

A

STAGE 3: CIRRHOSIS •Irreversible:

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32
Q

What are other causes of cirrhosis?

A

cholesterol non-alcoholic liver disease hepatitis metabolic disorder

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33
Q

What are the causes of ascites ?

A

portal hypertension liver cancer cardiac failure

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34
Q

What is hepatocellular carcinoma?

A

primary malignant tumour arising from liver epithelial cells (hepatocytes)

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35
Q

What are the two types of gallstones?

A

pigment cholesterol: bile salts : phospholipids

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36
Q

What is the acute GALLSTONE complication?

A

ACUTE **Clinical SSx - Sudden onset RUQ pain, +/- Rt shoulder referral•+/- fever or chills - Murphy’s sign: tenderness on RUQ palp., worse w. inspiration CHRONIC Infection - empyema acute pancreatitis coledocholithiasis (stone stuck in bile duct)

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37
Q

definition of constipation?

A

bowel movement less frequent to pass. ***consistency > frequency

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38
Q

Management for constipation?

A

Visceral techniques *** patient education may result in diarrhea and flatulence **** Increase fibre and water Introduce exercise

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39
Q

What are the different types of laxatives

A

First line: - Bulking agents - osmotic laxatives stool softener bowel stimulant opioid antagonist

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40
Q

Common causes of acute and Chronic diarrhoea ?

A

ACUTE infectuous gastroenteritis: salmonella, E.coli diet drugs Chronic infective diarrhoea Intestinal disorders Adverse drug reactions (alcohol)

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41
Q

Management for diarrhoea

A

Antibiotics (bacterial) Anti- diarrhoea agents opioids: act on GIT opiod receptor

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42
Q

Clinical features of IBS

A

abdominal Pain Rt/Lt iliac region. Variable bowel habit **diagnosis of exclusion*

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43
Q

Management for IBS?

A

food elimination process Pharmacology: Serotonin: - 5hT4 agonist - diarrhea - 5hT3 antagonist - constipation Antispachmodic - muscarinic receptor

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44
Q

What is diverticular disease?

A

diverticular disease= diverticulosis if pouch inflamed = diverticulitis

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45
Q

complication of diverticular disease

A

fistula: the connection between 2 organs Abscess formation: palpable mass leads to **peritonitis

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46
Q

What is Haemorrhoids

A

Internal haemorrhoid: varicosity of the superior rectal vein (proximal to pectinate line) External haemorrhoid: varicosity affecting the perianal venous plexus (distal to pectinate line)

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47
Q

What are the classifications of haemorrhoids

A

First degree Vein is distended and may bleed, but remains internal Second-degree Prolapse during defecation, but spontaneously reduce Third-degree & fourth-degree Remain protruding after defecation

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48
Q

Management of haemorrhoids?

A

Ointment: corticoid steroid Hydrocortisone/Cinchocaine

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49
Q

complications of hemorrhoids

A

strangulation thrombocis fibrosis persistent blood loss

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50
Q

Pathophys of apendicitis

A

Obstruction of the lumen prevents proper drainage As mucosal secretions continue, intraluminal pressure increases (decreases mucosal blood flow) Hypoxia-induced ulceration promotes bacterial invasion Gangrene Complications: Peritonitis, abscess formation

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51
Q

Clinical features for appendicitis

A

abdominal P: gastric + periumbilical region visceral P RLQ vomiting nausea anorexia fever diarrhoea or constipation

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52
Q

Aetiology for Ulceritive colitis

A

Form of IBD wiht ulceration caused by Autoimmune dysfunction

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53
Q

What is crohns disease?

A

A chronic inflammatory disorder that can affect any part of the GIT from the mouth to the anus

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54
Q

Pathophys of crohns disease

A

Most common sites: terminal ileum, ascending colon & transverse colon Chronic inflammation leads to the development of ***granulomas*** (clusters of modified macrophages)** ***cobblestone appearance**

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55
Q

Clinical features crohns?

A

Diarrhoea weight loss abd p malabsorbtion of small bowel

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56
Q

Complicaitons of ulceritis colitis and chrons

A

UC - toxic megacolon Crohns - anal fissure and fistula

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57
Q

Meds for IBD

A

Anti-inflammatory: - Corticosteroids - 5-AMinosalicylic acid Biological agents anti TNF bodies

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58
Q

Management crohn

A

dietary change

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59
Q

What is pernicious anemia?

A

autoimune gastritis - leads to V12 insufficiency

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60
Q

What are the types of oesophageal cancer

A

squamous cell carcinoma middle 1/3 adenocarcinoma lower 1/3

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61
Q

What is the classic triad of oesophageal cancer

A

Painful, difficult swallowing dysphagia odyphagia weight loss

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62
Q

What pathogen is causes stomach cancer?

A

Adenocarcinoma by H. pilori bacteria infection

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63
Q

What are the dramatic clinical features of stomach cancer?

A

haematemesis, melena, pyloric obstruction

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64
Q

cirrhosis complications?

A

portal hypertension hepatocelullar failure

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65
Q

what are the complications of cystic fibrosis (colestasis) ?

A

second biliary cirrhosis cholelithiasis

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66
Q

what is the pathogen for bowel cancer?

A

colorectal carcinoma

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67
Q

What is the ateology for bowel cancer ?

A

diet smoking IBS Family Hx

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68
Q

How is a lymphadenopathy classified?

A

Localised: 75% one body part

general: 25% population 2 or more areas = underline disease

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69
Q

What leads to splenomegaly?

A

INFECTIONS

HIV

PORTAL HYPERTENSION

LYMPHOID DISORDERS

RBC DISORDERS

INFLAMMATORY CONDITIONS

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70
Q

What is another name for glandular fever and what is its pathogen ?

A

infectuous mononucleosis caused by

Epstein-Barr Virus (EBV)

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71
Q

how do you diagnose glandular fever?

A

serologic testing to diagnose

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72
Q

What is leukaemia?

A

Proliferation of malignant leucocytes in the bone marrowOvercrowding causes malignant cells to spill into blood

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73
Q

What is lymphoma?

A

Proliferation of malignant lymphocytes in lymphatic systemFormation of discrete tumours

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74
Q

What is multiple myeloma?

A

Proliferation of malignant plasma cells in the bone marrow

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75
Q

How is leukaemia classified?

A

Lymphoid leukaemiaMyeloid leukaemiaAcute leukaemia – rapid growth of immature cells (referred to as ‘blasts’)Chronic leukaemia : slow growth

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76
Q

What are the 4 types of leukaemia?

A

Acute lymphoblastic leukaemia (ALL)Acute myeloid leukaemia (AML)Chronic lymphocytic leukaemia (CLL)Chronic myeloid leukaemia (CML)

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77
Q

what is the Aetiology of leukaemia?

A

combination of genetics environmental risk factors

chemo

genetic

smoking

radiation

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78
Q

What are the clinical features of leukaemia?

A

Anaemia

Decreased immunity (↓normal WBCs)

Splenomegaly, hepatomegaly, lymphadenopathy

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79
Q

Management for acute Leukaemia?

A

blood marrow biopsy + combination of chemotherapy.

DNA inhibitors cytaribine

RNA inhibitors daunorubicin

vincristine - mitosis inhibitor

radiotherapy after remision

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80
Q

What are the clinical features of chronic leukaemia?

A

acute blast crisis

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81
Q

Management for chronic Leukaemia?

A

CLL: chemotherapy and antibodies

CML: tyrosine kinase inhibitors

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82
Q

How is lymphoma classified?

A

Hodgkin’s lymphoma Non-Hodgkin’s lymphoma

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83
Q

Risk factors for lymphoma?

A

Family history

Certain infections

ObesityIa

iatrogenic immunosuppression Autoimmune conditions:

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84
Q

Clinical features of hotchkins lymphoma?

A

no spread Lymphadenopathy single or chain related nodes

red sternberg cell

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85
Q

pathogen atributed to non-hotchkins lymphoma?

A

B cell neoplasm

T cell and NK cell neoplasm not as common

originates in multiple sites cervical axillary etc

spread is common

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86
Q

Pathophysiology of multiple myeloma?

A

Myeloma cells: (M proteins) Result: decreased immunity,

Antibody fragments (light-chains) Result: amyloidosis leads to renal failure

plasmacytomas destroys bone Result: radiographic ‘punched-out’ lesions (1-4cm in diameter)

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87
Q

What is HIV?

A

HIV is the pathogen responsible for acquired immunodeficiency syndrome (AIDS)It is a retrovirus and carries its genetic material as RNA (not DNA)

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88
Q

Modes of transmission of HIV?

A
  • Exchange of body fluids- Children infected in placenta- occupational exposures

Not transmited by: touch

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89
Q

What is the pathophysiology behind HIV?

A

Entry into cell HIV binds to CD4 receptor and chemokine co-receptor

Conversion of viral RNA

viral enzyme protease modify new virons

CD4 glycoprotein depletion = kill T/ B lymphocites

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90
Q

Stages of HIV

A

STAGE 1: ACUTE INFECTIONSTAGE 2: CHRONIC INFECTION (CLINICAL LATENCY)STAGE 3: ACQUIRED IMMUNE DEFICIENCY SYNDROME

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91
Q

Management of HIV

A

Antiretroviral medications - prevent progresion

MAINTAIN PHYSICAL & MENTAL HEALTH:POST-EXPOSURE PROPHYLAXISPRE-EXPOSURE PROPHYLAXIS

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92
Q

What are the two types of UTI

A

Lower UTI - •urethritis, cystitisUpper UTI - •= pyelonephritis

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93
Q

Define UTI?

A

•Presence of more than 100,000 organisms per ml (105/ml) in a Mid-Stream Urine (MSU)specimen.

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94
Q

What is the incidence for UTI?

A

Woman pregnancy

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95
Q

What is the organism responsible fr UTI?

A

E.Coli

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96
Q

What are the risks for UTI?

A

Sexual intercorse pregnancy changes in the balance of the commensal organism neonatesdiabetes melileusimmunosuppressors bladder instrumentation lower urinary tract obstruction

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97
Q

What are the clinical features of Lower UTI?

A

Urethritis * dysuria * Pain during urination Cystitis * pain during voiding * The sensation of a full bladder Foul smell urineHematuriaFever In elder: fatigue confusion

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98
Q

WHat is an upper UTI?

A

•An infection can ascend and cause an acute pyelonephritis if the vesico-ureteric valves are incompetent and/or the bacteria can climb

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99
Q

What is the pathophysiology of upper UTI?

A

•Spread of the infection further into the kidney an occur via two routes: * •Directly through the lumen of the collecting tubules * •Passing from the submucosa of the inflamed calyces into the interstitial tissue •Organism proliferation incites an acute inflammatory reaction •Abscess formation is possible and associated with renal damage

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100
Q

Clinical features of Upper UTI?

A

•Sudden onset of unilateral or bilateral loin pain +/- radiations occurs to the iliac fossa and groin•Tenderness/guarding are usually present in the renal angle and lumbar region•Fever, rigors, nausea, vomiting can occur•Symptoms of the initial cystitis:urinary frequency, dysuria, cloudy, offensive–smelling urine

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101
Q

What is the management for UTI?

A

Urine test Antibiotic therapy PTE education Address risk factors

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102
Q

What is Nephrolithiasis?

A

Kidney stonesmasses of minerals that cause urinary obstruction

103
Q

What are the types of renal calculi?

A

•75-85% of calculi are composed of calcium oxalate and phosphate •5-10% are uric acid stones •5% are composed of struvite •1% are cystinestones

104
Q

What are the risk factors for renal calculi?

A

* Hot weather * increase sweating * decrease fluid intake * Diseases with increase stone forming minerals * Increased dietary intake of stone forming minerals * correlation with chronic disease (HBP, obesity, diabetes,)

105
Q

What is the pathophys for kidney stones?

A

* deposit of calcium phosphate (rnadal’s plaques) * plaques move into urinary lumen acting as nuclei for growth * aggregation of mineral leads to stone

106
Q

Clinical features of kidney stones?

A

dull flank pain pain may radiate to the groin pain exacerbated by urination hematuria or stony fragments in urine renal distention asymptomatic

107
Q

What are the complications of renal calculi?

A

Ureteric impaction: renal colic * pallor * sweating * vomiting * crying agony Neoplasia: •Large stones can Irritate the renal epithelium causing metaplasia, and eventually squamous cell carcinoma

108
Q

What is the ureteric referred pain pattern?

A
109
Q

What is the management of kidney stones?

A

Pain managementreduce the concentration of stone-forming substances removal of stone * ureteroscopy * lithotripsy - laser

110
Q

What is chronic kidney disease?

A

The decline in kidney function 69-80 mild <15 = kidney failure

111
Q

Aetiology of kidney failure?

A

* Systemic disease: diabetes HBP * renal disease: kidney stones/ chronic pyelonephritis

112
Q

Pathophys of kidney disease?

A

Intact nephron hypothesis * •Surviving nephrons compensate for damaged nephrons until the advanced stages of CKD * •These nephrons undergo expansion and are capable of hyperfiltration Trade off hypothesis * •The continued loss of functioning nephrons and adaptive hyperfiltration likely results in further nephron injury and ultimately end-stage disease Pathological processes of CKD * •Progressive glomerular hypertension, hyperfiltration and hypertrophy * •Glomerulosclerosis * •Tubulointersitial inflammation and fibrosis

113
Q

Clinical features of kidney failure?

A

MUSCULOSKELETALCHANGES * •Bone pain, * increased # risk, * m. weakness, * myalgia, * arthralgia NEUROLOGICAL CHANGES * •Peripheral neuropathies (esp. sensory in lower limb) * •Cognitive or behavioural effects * Neuromuscular irritation: muscle cramps, twitching

114
Q

MAnagement for kidney failure?

A

DIetary managementmedication KIDNEY FAILURE * dialysis * renal transplant

115
Q

What is AKI?

A

•Sudden decline in kidney function occurring over hours to days•Results in reduced fluid & electrolyte regulation, waste elimination and acid-base balance

116
Q

What are the classifications of AKI?

A

* prerenal: impaired renal blood flow * intrarenal: nephron damage (infection) - least likely for osteos * postrenal: urinary tract obstruction

117
Q

What is Bladder cancer?

A

Primary cancer that starts in the bladder. * Transitional cell carcinoma

118
Q

Risk factors for bladder cancer?

A

* smoking * chemicals * family Hx

119
Q

What are the clinical features for bladder cancer?

A

HematuriaUrinary symptomspainabdominal masssystemic featureshepatomegaly

120
Q

What is the most common type of kidney cancer?

A

renal cell carcinoma

121
Q

Risk factors for renal cancer?

A

* male * smoking * chronic disease * chemicals * Family Hx

122
Q

Clinical features of kidney cancer?

A

* haematuria * flank pain * abdominal mass * systemic features * metastatic disease

123
Q

What is menopause?

A

cessation of menses for 12 consecutive months

124
Q

What is the physiology of menopause?

A

* •As ovarian follicles diminish with age, so too does the amount of oestrogen produced by granulosa cells * •BecauseLH secretion isdependent on oestrogen levels, menopause is preceded by ~5 years of increasingly anovulatory cycles (referred to as the climacteric) * •Eventually, menstruation ceases due to reduced number of follicles & reduced responsiveness to FSH * •Average age for cessation of menses: 51 years

125
Q

What are the clinical features of menopause?

A

Non-specific - hot flushes, hight sweat, fatigue, lethargy reproductive: reduction fo breast size, vaginal dyspareunia, UTI Neurological: changes mood and memory, headache, dizziness Musculoskeletal: osteoporosis, arthralgia, myalgiacardiovascular: HBP, AMI

126
Q

what is the climacteric period?

A

period with irregular menses before complete cessation of menstruation

127
Q

What are the advantages and disadvantages of hormone therapy?

A

ADVANTAGES * •Relieves symptoms of menopause * •Prevents early menopausal bone loss – reductionin #risk DISADVANTAGES * •‘Premenstrual-like’ symptoms e.g. bloating & fluid retention, breast tenderness, irritability •Increased risk for: * •Thromboembolic disease * •Cardiovascular disease: stroke * •Cancer: breast, endometrial (oestrogen-only HT) * •Gall bladder disease

128
Q

What is Polycystic ovarian syndrome?

A

Inappropriate secretion of gonadotrophinsDiagnostic criteria * menstrual irregularity * clinical hyperandrogenism * polycystic ovaries

129
Q

What is the correlation between PCOS and Chronic disease?

A

Hyperinsulanemia

130
Q

What is the pathophys behind PCOS?

A

* •Follicular growth is continuously stimulated, but not to full maturation * •Hyperinsulinaemia suppresses normal follicular apoptosis – this permits the survival of follicles that would normally disintegrate * •The net result is anovulation and enlargement of the ovaries with cyst formation

131
Q

What are the clinical features of PCOS?

A

* •Menstrual disturbance: oligomenorrhoea, amenorrhoea * •Infertility * •Hyperandrogenism: acne, hirsutism, male pattern baldness * •Obesity (38% of cases) * •Asymptomatic (20% of cases) * •Increased risk for: Type 2 diabetes, cardiovascular disease, endometrial cancer

132
Q

Management of PCOS?

A

combined oral contraceptiveanti-androgen agentsInsulin sensitisers

133
Q

What is Pelvic inflammatory disease (PID)?

A

ANy infection in the genitourinary tract which was not treated.

134
Q

WHat are the risk factors for PID?

A

Sexually active womenInadequately treated chlamydia or gonorrheasurgical procedure: IUD, Abortion, C-section

135
Q

What are the clinical features for PID?

A

Low abdominal painirregular bleedingmucopurulent discharge

136
Q

What are the complications fro PID?

A

* infertility * •Pelvic adhesions * •Abscess formation * •Ectopic pregnancy * •Chronic pain

137
Q

What is the management for PID?

A

antibioticsSurgery

138
Q

what is endometriosis?

A

deposits of endometrial tissue found anywhere except the uterine mucosa.related to vicarious bleeding

139
Q

Where are the posible sites for vicarious bleeding related to endometriosis?

A

Common: * uterine tube * uterus * bowel * bladder * ureters Post surgery: vagina, perineumRare: umbilicus, inguinal canalvery rare; pleura, diaphragm, nose

140
Q

What are the 3 possible pathophys mechanisms for endometriosis?

A

Retrograde menstruationembryonic cellsendometrial emboli

141
Q

Clinical features related to endometriosis

A

•Pain: pelvic pain, dysmenorrhea, dyspareunia•Bleeding: menorrhagia, irregular periods, spotting•Bowel or bladder symptoms: dysuria, dyschezia, ‘cyclical’ IBS symptoms•Reduced fertility•Systemic: fatigue, lethargy, depression

142
Q

what is the management of endometriosis?

A

•Analgesia•Suppression of ovulation e.g. COCP•Laparoscopic ablation of ectopic tissue, adhesions looks to restore fertility and reduce spread of tissue

143
Q

What is a uterine fibroid (leiomyoma)?

A

A common, benign tumour arising from the smooth muscle cells of myometrium

144
Q

What is the pathophys behind uterine fibroids?

A

•Myomas are usually spherical•Some extend out on stalks (pedunculated)•There may be multiple (in some cases up to 200!)•The fibroid develops in the myometrium and can remain there•Alternatively, it can protrude into the uterine cavity (submucosal fibroid) or out of the perimetrium (subserosal fibroid)

145
Q

What are the clinical features of fibroids?

A

* •Bloating, * palpable mass, * protruding belly, * sensation of abdominal heaviness * •Dysmenorrhea or menorrhagia (can lead to iron deficiency anaemia) * Pressure on surrounding organs

146
Q

What are the complications of fibroids?

A

•Torsion: twisting on their stalks (pedicles)•Ulceration & bleeding •Small risk of malignant change (to uterine sarcoma)

147
Q

What is the most common type of uterine cancer?

A

adenocarcinoma: •Develops from the secretory epithelium of the endometrium

148
Q

What are the risk factors for uterine cancer?

A

Exposure to oestrogenObesity family Hxprevious pelvic radiation for cancer

149
Q

What are the clinical features for uterine cancer?

A

irregular vaginal bleedingvaginal discharge: watery brownlower abdominal painspread of tumour

150
Q

What are the types of ovarian cancer?

A

epithelial type: arise from a germ cell type.rarely primary tumour mostly arise from breast cancer.

151
Q

What are the risk factors for ovarian cancer?

A

Agefamily HxOestrogen

152
Q

What are the clinical features of ovarian cancer?

A

Pain or pressure on the back, abdomen and pelvisabdominal bloatingindigestion/ nauseaurinary frequency and urgency hormone-secreting tumour

153
Q

What are the types of cervix cancer?

A

squamous cell carcinoma

154
Q

What are the clinical features fro vaginal cancer?

A

Asymptomaticvaginal discharge with a foul odour abnormal bleeding pelvic pain symptoms of compression of bladder discomfort.

155
Q

What are the possible spread sites if vaginal cancer is not detected?

A

•Direct spread: Through the uterine/vaginal walls to adjoining organs•Lymphatic spread: To pelvic, inguinal, iliac and aortic nodes•Blood spread: to the liver, lungs and bone

156
Q

What is the management of vaginal cancer?

A

Early vaccination HPV test - if positive do Pap smear

157
Q

What is the two-tiered classification system of the squamous intraepithelial lesion (vaginal cancer)r?

A

•CIN 1 was renamed Low-grade Squamous Intraepithelial Lesion (LSIL)•CIN 2 & CIN 3 were renamed High-grade SILs (HSIL) – Surgery

158
Q

What is a venerial disease

A

STI

159
Q

What are the female defences against infections

A

* •Normal defences of the female GUT include: * •Oestrogen & lactobacilli * •Thick vaginal epithelium * •Cervical mucus plug * •Regular shedding of endometrium

160
Q

WHat are the defenses of the male reproductive tract?

A

* •Normal defences of the male GUT include: * •Prostatic secretions * •Confer a degree antimicrobial activity * •Increasedlength of the male urethra * •A drier peri-meatalenvironmentcompared to women

161
Q

What are the complications of STI?

A

* •Malignancy, * Infertility, * Ectopic pregnancy, * PID, * Neonatal morbidity * mortality

162
Q

What are the contributing factors for increased incidence of STI?

A

* Sexual freedom * change in perceived sexual risk * increased travel * use of recreational drugs * less barriers for contraception

163
Q

What is Chlamydia?

A

Bacterial STI caused by Chlamydia trachomatis bacteria.lives and multiply within cell incubation for 14 days

164
Q

What is the pathophys of clamydia?

A

WOMEN: * •Cervix affected more than vagina * •Chronic cervicitis, even salpingitis can develop * •Complications: ectopic pregnancy, infertility MEN: * •Typically develop urethritis * •Women & MSM who engage in receptive anal intercourse may develop an infection in the rectum * •It is possible for the conjunctivae* and oropharynx to be infected through direct inoculation * •*Leading cause of infectious blindness in the world

165
Q

What are the clinical features of clamydia?

A

WOMEN: * •Vaginal discharge, * bleeding, * abdominal pain, * bloating, * dyspareunia MEN: * •Dysuria is more common, * there may be a penile discharge OTHER SITES OF INFECTION: * •Proctitis, * pharyngitis, * conjunctivitis 8% of patients develop a reactivearthritis

166
Q

What is gonorrhoea?

A

STI bacteria caused by Neisseria gonorrhoeae3-7 incubation day

167
Q

What are the clinical features of gonorrhea?

A

•Rectal infection * •Proctitis:rectal pain * tenesmus, * anal discharge * •Asymptomatic •Pharyngealgonorrhoea * •Most commonly asymptomatic * •+/- cervical lymphadenopathy •Conjunctivitis: * •Copious amounts of exudate, bright red or “beefy” conjunctivae * •Serious complications: cornealulceration and visual deterioration * Mother-to-child transmission during vaginal delivery can occur

168
Q

What is reactive arthritis?

A

a complication of chlamydial & gonorrhoeal infection related too oligoarthritis on •knees, SIJs, interphalangeal joints, LBPmay affect Aquiles tendon

169
Q

What are the clinical features for the 3 types acquired syphilis?

A

Primary syphilis: * Symtoms 2-4 weeks * chancre in: penis, cervix, vagina, anus, oropharynx * chancrea may heal without treatment Secondary syphilis * 6-8 weeks * rash * wart like lessions * silvery gray lesions * systemic symptoms * lymphadenopathy Tertiary syphilis * 10 to 25yr * Gummas: skin, mucous membranes, bone neurosyphilis: * •Mild symptoms: Headaches, photophobia, dizziness, blurred vision, poor concentration •Severe symptoms: Meningitis, seizures, paraplegia, psychosis, cognitive decline * cardiovascular features: Gummas in the myocardium

170
Q

WHat is the causitive agent of genital herpes?

A

Herpes simplex type 2 transmitted through genital or oral contactbecomes active 2-3 times a year

171
Q

clinical features of herpes simplex?

A

* Group tender vesicles at •penis, labia, perianal skin, buttocks •Intense burning stinging •Fever, lethargy HVS nerve root progression * •First attack:lasts 2-4/52 before lesions crust and disappear * •There may be recurrences, which typically last for 7-10 days

172
Q

What is vaginal Thrush?

A

overgrowth of the fungus CandidaalbicansArises from disordered local ecology that allows the overgrowth of the yeast •Factors that can change vaginal microbiome: * •Pregnancy, * diabetes, * antibiotic therapy, * some types of OCP

173
Q

What is toxic shock syndrome?

A

a form of septic shock (circulatory failure), secondary to bacterial infection and toxin releaseCausative agent: •Staphylococcal aureus +, Streptococcus pyogenes Cause: tampons + low menstrual flow while using tampons may cause vaginal lesions

174
Q

What are the clinical features and complications of septic shock?

A

Clinical features * •Abrupt onset: high fever, vomiting, diarrhoea * •Also common: sore throat, myalgia, headaches, skin rash Complications * septic shock

175
Q

What is acute prostatitis and its classifications?

A

acute inflammation of the prostateNon-bacterial prostaitis: trauma, infectionBacteria prostaitis: E coli, clamydia, gonorrhea

176
Q

what is the clinical presentation of prostatitis?

A

Paindysuriaobstructive voidingirritative voiding ***Infective prostatitis: fever, chills

177
Q

What is benign prostate hyperplasia BPH?

A

hyperplasia of stroma affects transition zone affects old men

178
Q

what is the enzyme related to BPH?

A

5a reductase (an enzyme that converts testosterone to DHT)responsible Dihydrotestosterone DHT

179
Q

What area of the prostate does BPH affect?

A

transitional zone

180
Q

what are the clinical features of BPH?

A

Obstructive symptom (affect urine flow and stream)Irritative symptoms (affect urine urgency, frequency, night pee)

181
Q

what are the complications fo BPH?

A

Bacterial infection bladder stonesbladder diverticuli

182
Q

What are the managements for BPH?

A

Meds: 5-alpha-reductase inhibitor surgery

183
Q

What is the pathogen responsible for Prostate cancer?

A

adenocarcinoma

184
Q

what is the aetiology of prostate cancer?

A

Old, obese, male smoker with diabetesloves BBQworks with chemicalsgenetics Hormonal factors

185
Q

Where is the first spread zone for prostate cancer and how?

A

spine via blood and lymphs

186
Q

how do prostate cancer tumours affect bones different to other cancers

A

(tumours in bones)cause secondary osteoblastic that are dense and easy to detect in x-rayThis is the only detectable site of metastasis

187
Q

What are the clinical features for prostate cancer?

A

asymptomaticObstructive and irritative symptomsOthers * hematuria * pain * systemic * DRE * Bone #

188
Q

What is TURP?

A

removal of the prostate via rectumtransurethral resection of prostate

189
Q

Management for prostate cancer?

A

Surgery (TURP or Open)Radiation (needle vs seed brachytherapy)

190
Q

what is an inguinal hernia and how is it classified?

A

protrusion fo abdominal content into inguinal canalindirect - inside canal via deep inguinal ring direct - posterior wall of canal (weakness in transversalis fascia

191
Q

what is the risk of getting an inguinal hernia?

A

male 27%female 3%Profile * old man, tradie/ athlete, smoker with high BMI

192
Q

what are the clinical features

A

lump in groin and discomfort in abdomen

193
Q

Define Hydrocele?

A

accumulation of fluid in Tunica vaginal

194
Q

how are hydrocele classified?

A

Primary hydrocele: fluid not reabsorved Secondary: excess fluid from infection congenital: conection between vaginalis and abdomen not closed

195
Q

What is Cryptorchidism?

A

failure of testicles to descend from abdo to scrotum.

196
Q

Where is the most common arrest site of testes in cryptorchidism?

A

inguinal canal

197
Q

what are the complications in cryptorchidism?

A

inguinal hernia infertility testicular cancer

198
Q

What is the management for cryptorchidsm?

A

surgery - orchiopexy

199
Q

What is the venous drainage for the testes and epididimis?

A

pampinfon plexus drains into testicular vein in abdo

200
Q

What is varicocele and how are they classified?

A

varicosity of the testicular and pampiniform plexus primary: incompetent valvesSecondary: pathological condition

201
Q

What is testicular torsion?

A

twisting of sperm cord***its a medical emergency*** may lead to infarction, must be fixed 6 hours after onset to avoid ischaemic necrosis

202
Q

what is the most common cause of testicular torsion?

A

congenital malformation of tunica vaginalis “bell-clapper abnormality”

203
Q

Who is the most affected population with testicular torsion?

A

Adolescents

204
Q

What are the 2 main varieties of testicular cancer ?

A

seminomas: cancer in seminiferous tube - common non semionmas: mixed germ cell - aggressive

205
Q

What is the incidence and risk factors of testicular cancer ?

A

seminomas: adult 25+non-seminoma: young adult 20’s Risks * family Hx * cryptorhidism

206
Q

what are the clinical features for testicular cancer?

A

large testiclessensation of “heavy” scrotum”asymptomatic metastatic diseasesecondary hydrocelegynaecomastia (large man bobs’)

207
Q

what is the management for testicular cancer

A

surgery - radial orchiectomy

208
Q

What are the effects of insulin?

A

Carbs: Liver: + storage of glucose as glycogen Fats: Adipose tissue: +conversion of glucose to fatProteins: - glucogenesys + Cellular uptake of AA

209
Q

What are the effects of lack of insulin?

A

Fats: used as fuel sourceProtein: AA used as fuel

210
Q

What are the effects of glucagon?

A

Affect liver - breakdown glycogen (glycogenolosis)- Synthesis of glucose (gluconeogenesis)Lower blood levels of AA

211
Q

What messenger does glucagon use to act?

A

second messenger

212
Q

What is diabetes?

A

clinical syndrome characterised by hyperglycaemia due to absolute or relative insulin deficiency

213
Q

How is diabetes diagnosed?

A

blood sugar > 11.1fasting sugar> 7HbA1c>6.5

214
Q

What are the classifications of diabetes?

A

Primary- diabetes type 1: Absolute deficiency (insulin dependant) 10% adults- diabetes type 2: relative deficiency 88% adults Secondaryarises from known pathology

215
Q

what is pre-diabetes?

A

Impaired glucose tolerance***levels higher than normal but not high enough to be diabetes**

216
Q

What causes diabetes type 1

A

Genetics: Environmental factors Autoimune T1DM Virus: rubella, epstein barr, cytomegalovirus

217
Q

What causes diabetes type 2

A

Old, fat, lazy, smokersGenetics T2DM

218
Q

What is oxidative stress and what pathology is associated to?

A

stress fat tissues: releases cytokines which in T2DM impair insulin receptors = target cells less responsive also damage beta cells in pancreasObesity associated with decrease insulin receptor density

219
Q

What type of insulin deficiency is T1DM related to?

A

absolute deficiency (type 1 diabetes)

220
Q

What type of insulin deficiency is T2DM related to?

A

Diabetes type 2 - relative deficiency = insuline resistanceprocess: target cells become resistant initial stage: hyperinsulinaemialater stage: beta cell exhaustion leads to insulnpaenia

221
Q

what are the clinical features for type 1 diabetes mellitus (T1DM)

A

polyphagia (gluttony with no wight gain)polyuria (fast pee) polydipsia (thirst)Glycosuria (sugar in pee)

222
Q

what are the clinical features for type 2 diabetes mellitus (T2DM)

A

hyperglycaemia glycosuria+ risk infection

223
Q

What are the complications for diabetes?

A

Acute- hypoglycaemia (low sugar) - Ketoacidosis (body can’t produce insulin)Chronic- vascular disease- diabetic neuropathy - diabetic foot (no feeling on foot)

224
Q

What are the clinical features for hypoglycaemia?

A

CNS: fatigue HA drowsiness, speech problemANS: sweating, trembling, pounding heart, hunger Severe hypo: coma, convulsion, brain damage

225
Q

What are the complications of Diabetic ketoacidosis (DKA)

A

deathKetone acidosis (decrease PH)

226
Q

What are the clinical features of ketoacidosis?

A

***MEDICAL EMERGENCY***hyperglycemiaacetone breathrespiratory compensationmental disturbancepheripheral vasodilation

227
Q

What is diabetic vascular disease and what are its complications?

A

group of blood vessel pathologiesatherosclerosis = diabetic Macroangiopathy (large vessel)Arteriosclerosis = diabetic microanginiopathy (capillaries)

228
Q

What are the chronic complications of diabetic foot?

A

low limb amputationgangrena - necrosis

229
Q

What is the first line pharmachological management of T2DM?

A

biguanides + glucose uptake- glycogenesis - intestinal absorption

230
Q

Thyroglobulin is the percursor for which thyroid hormones?

A

T4 - T3

231
Q

What do parafollicular cells secrete

A

calcitonin

232
Q

How are thyroid hormones classified?

A

Aminoacidscontain iodine

233
Q

What receptor does TSH bind to?

A

follicular cell receptors

234
Q

What are the effects of thyroid hormones?

A

gene transcriptioncatecholamine effect regulate normal function

235
Q

What is nontoxic goitre?

A

enlargement of thyroid gland - normal function maintained

236
Q

What is the cause of goitre?

A

iodine deficiency

237
Q

What is hypothyroidism?

A

Deficiency of T3 and T4 in fetes leads to intelectual disability “cretinism”

238
Q

How is hypothyroidism classified?

A

Primary: failure of thyroid - Hashimoto (autoimune) Secondary: TSH deficiencyTertiary: TRH deficiency

239
Q

What is hashimoto thyroids

A

primary type thyroidism • Autoimmune disorder characterised by lymphocyte-mediated inflammation and fibrosis

240
Q

What is chronic lymphocytic thyroiditis?

A

Secretion of IgG anticoagulant affecting - thyroglobulin- thyroid peroxideEarly disease: leads to goitre

241
Q

What are the clinical features for chronic lymphocytic thyroiditis?

A

goitre- metabolic rate GAG - skin accumulation **may lead to myxoedema and increase risk of angina**

242
Q

Whta hormone replacement therapy is used for Lymphocytic thyroids?

A

levothyroxine

243
Q

What is thyrotoxicosis?

A

thyroid hormone excess “graves disease”

244
Q

What is the pathophysiology of graves disease?

A

Antibodies affect TSH receptors (TSHrAbs)+ levels T4 & T3produce goitre antibodies fluctuate with severity of disease

245
Q

What are the clinical features of Thyroxicosis?

A

+ metabolic rate+ apetite & thirst+ palpitationsnervousness/ psychosismenstrual irregularitiesloss of libido

246
Q

Clinical features for graves disease

A

ocular changes - eyes pop outskin changes= GAG in legs

247
Q

Management of graves disease

A

any thyroid drugs PTU - reduce thyroid peroxidase

248
Q

What is the most common type of thyroid cancer?

A

papillary carcinoma

249
Q

what are the risk factors for thyroid cancer?

A

radiation Family Hxbenign thyroid disease

250
Q

What are the clinical features for thyroid cancer?

A

enlarge nodule, firm not tenderneck discomfort due to pressure

251
Q

Management for thyroid cancer?

A

thyroidectomy - surgery

252
Q

What is the function of parathyroid glands

A

secrete parathyroid hormone PTH which increases plasma levels of Calcium Ca2.If Ca2 is high PTH is inhibitedPTH + renal excretioncalcitonin pose PTH actions on bone

253
Q

What are the clinical features of hyperparathyroidism?

A

hypercalcaemia-bones- stones- abdo groans + BP

254
Q

What are the clinical features of hypoparathyroidism?

A

hypocalacemia+ excitability of sensory and motor nerves- BP

SBO5 (16 decks)

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